































Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023


Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

7 
 

 

Protective Roles of Quercetin, Vitamin C and 

Pyridoxine on Lead Neurotoxicity via Enhanced 

Haematopoietic and Antioxidants Components 

 

By 

Nnachi Ifenna Salvator, Elizabeth Finbarrs-Bello, Ozor 

Ignatius Ikemefuna, Mba Christian Ejuiwa, & Vivian Ugwu 

 

Abstract 

Background: The harmful effects of lead exposure, especially its effect on the nervous system, 

raise serious concerns worldwide. This study is aimed at evaluating the effect of Quercetin, 

Vitamin C and Pyridoxine on Haematology, biochemical and histology of the cerebral cortex 

on lead induced neurotoxicity using adult Wistar rat models. Materials and Methods: Forty 

male Wistar albino rats were divided into five groups: control, lead only, lead + Quercetin, lead 

+ Pyridoxine, lead and Vitamin C. 100mg/kg/bw of lead was used to induce-toxicity for 7 days 

and treated with the following: Quercetin, Pyridoxine and Vitamin C were administrated orally 

respectively for 14 days. Hematological and biochemical samples were collected in three 

phases. The cerebral cortex was examined under light microscopy after H&E staining. Results: 

lead decreased all hematological parameters (PCV, WBC, RBC, HB and Platelets) examined 

and in the biochemical parameters, decreased slightly SOD, increased MDA and reduced 

significantly (p values) GSH. Quercetin, Vitamin C and Pyridoxine had strong curative effects 

on both hematological and biochemical parameters. On the histology, lead revealed mild glial 

cell infiltration. All treatment groups showed normal neuronal cells. Conclusion: Quercetin, 

Vitamin C and Pyridoxine showed neuroprotective effects against lead-induced neurotoxicity; 

therefore, they can be used as routine supplements against lead toxicity in endemic 

communities. 

Keywords: Quercetin, Pyridoxine, Lead, Ascorbic acid, neurotoxicity, lipid peroxidation 

 

Introduction 

Lead (Pb) is one of the most widely used heavy metals, especially in batteries, 

paint pigments, and plastics. This heavy use has produced local and global 

contamination of the air, soil, and water originating from lead-based pipes. The 

effect of exposure to Pb vary from mild to severe, depending on the degree of 

exposure, and is referred to as lead toxicity (Raymond, 2011). The nervous 

system (central and peripheral components) is the primary target of lead 

poisoning or toxicity (Brent, 2006; Bellinger, 2004). Pb toxicity is also known 

to induce a broad range of hematological, biochemical, and histomorphological 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

8 
 

dysfunctions in lab animals and humans (Hsu & Guo, 2002; Pande & Flora 

2002). This is characterized by persistent vomiting, anemia, encephalopathy, 

lethargy, delirium, convulsions and coma, and death in extreme cases (Flora et 

al., 2006; Pearce, 2007). One of the possible mechanisms underlying Pb-

induced toxicity or poisoning is its ability to induce oxidative stress in blood 

and other tissues, which contributes to the pathogenesis of poisoning by 

interfering with the delicate prooxidant/antioxidant balance that exists within 

the mammalian cells. Several investigators suggest a possible involvement of 

reactive oxygen species (ROS) in Pb-induced toxicity (Adonaylo & Oteiza, 

1999; Pande & Flora, 2002; Hsu & Guo, 2002) where Pb increased lipid 

peroxidation indicator the malondialdehyde (MDA) and decreased the 

activities of antioxidants enzymes: glutathione peroxidase (GPx), and 

superoxide dismutase (SOD) in the rat brains (Kuhad & Chopra, 2007). 

Antioxidants have been identified to protect the neurons against various 

experimental neurode generative conditions (Kuhad & Chopra, 2007). Vitamin 

C, vitamins E and B6, zinc, and selenium are antioxidants used to reverse Pb-

mediated toxicity by ameliorating oxidative stress status (Hsu & Guo, 2002). 

Flavonoids have now become a topic of interest due to their beneficial effects 

on different diseases. Quercetin is a natural flavonoid, ubiquitously found in 

common fruits and vegetables such as onions, broccoli, and apples (Sriraksa et 

al., 2016). Studies have reported that quercetin exhibits substantial antioxidants 

property, has the ability to scavenge free radicals, and aids many biological 

processes involved in oxidative stress (Formica et al., 1995). This study, 

therefore, evaluates the hematological, biochemical, and histomorphological 

effects of Quercetin, Vitamin C and Pyridoxine on lead-induced neurotoxicity 

in adult Wistar rats. 

Materials and Methods 

Procurement of Compounds, Chemical and Drugs 

5g of Quercetin was procured from Zigma, Aldrich USA. Lead (Pb) weight of 

5.2g was procured from registered chemical store at Ogbete main market 

Enugu Metropolis, Nigeria. 5g of Vitamin C (ascorbic acid) and Pyridoxine 

(Vitamin B6) were procured from Omaryon group of companies Enugu 

Metropolis, Nigeria. 

Animal  Handling 

Forty (40) Wistar rats weighing between 150 - 250g were purchased from the 

animal house of the University of Nigeria, Nsukka, Enugu State, Nigeria. The 

rats were housed at the animal facility of the College of Medicine, Enugu State 

University of Science and Technology Enugu Nigeria. The rats were housed 

for a period of 4 weeks to attain desired weights and to get them acclimatized 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

9 
 

in their new environment. The rats were fed pelleted rat chow (Vital, Nig. Ltd.) 

and allowed water ad libitum. Thereafter, the rats were grouped into five (5) 

groups; each group had eight rats housed in two different cages 2 (n=4) per 

group. The rats were kept in ventilated cages at optimum temperature 28oC 

with 12 hours light/dark cycle, and humidity of 60%. The study was reviewed 

and approved by the Faculty Ethics and Research Committee. 

Induction of Lead Toxicity  

The used dose for lead induction was adopted from Highab et al., (2018), 100 

mg /kg/bw of lead was administered orally for 7days across groups. Thereafter, 

Quercetin was administered as modified using methods of Tian et al., 2019, at 

50mg /kg / bw). Vitamin C and Pyridoxine (Vitamin B6) were used as standard 

drug for the experiment, the doses were adopted from Razmkon et al., (2011) 

at dosage 500 mg /kg /bw for Vitamin C and 100 mg/ kg/ bwt for Pyridoxine 

(Vitamin B6).all treatment were administered via oral gavage for 14 days. 

Experimental Design 

 

Hematological and Biochemical Evaluations 

Blood samples were collected from all the rats thrice to form a baseline, after 

induction and after treatment as well as parameter for post induction. Materials 

used for collection of samples are; capillary tubes and plain EDTA bottles. The 

following were evaluated; PCV, WBC, RBC, HB, and Platelets for 

hematological studies using standard protocols. While serum Superoxide 

dismutase (SOD), Malondialdehyde (MDA) & Glutathione (GSH) antioxidant 

marker enzyme were determined using the respective kit in accordance with 

manufacturers recommended protocols (Fortress diagnostic limited UK). 

Measurement of Malondialdehyde (MDA), a prototype of the thiobarbituric 

reactive substances (TBARS) as a biomarker of lipid peroxidation and 

oxidative stress using modified thiobarbituric acid method (Todorova et al., 

2005).The IBM SPSS package (IBM Corp., IBM SPSS Statistics for Windows, 

Version 25.0, Armonk, NY, USA),was used to analyze the data. Descriptive 

statistics was evaluated for hematological and antioxidative markers and 

presented as means and standard deviations.  An analysis of variance test (One-

way ANOVA) was used for comparison of the means for the hematological, 

and antioxidant enzymes. The P values for comparing means were considered 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

10 
 

significant at p ≥ 0.05.  

Termination of Study and Tissue Collection 

On the 15th day (day one post treatment), the rats in all groups were sacrificed 

under light etherand the brains were harvested. The brains were fixed in 10% 

neutral formal saline for 48hrs. Thereafter the cerebrum were isolated for 

routine paraffin processing and stained with Haematoxylin and Eosin. 

Representative photomicrographs were captured after the interpretation. 

Results 

Hematological Analysis 

 

Figure 1: Shows PCV test results across groups. The PCV values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. In group E (Lead only), the PCV values 

regressed with continuous administration. Treatment groups B, C and D was 

observed to have increased PCV values after treatment which is similar when 

compared to observations in control group A. However, PCV values were not 

significant (P > 0.05) in paired sample correlations across groups in 2nd and 

3rd study. 

A B C D E

Baseline 48 64.33 51.33 52.66 64.6

PIS 57.33 41.33 41.66 41.33 41.66

Treatment 63.66 46.33 51.66 49.66 35

0
20
40
60
80

P
C

V
  P

ER
C

EN
TA

G
E

GROUPS

PCV (%)

Baseline PIS Treatment



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

11 
 

 

Figure 2: Shows WBC test results across groups. The WBC values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. In group E (Lead only), the WBC count was 

significantly lower (P < 0.05) compared to the control group A and treatment 

groups B, C and D. WBC values was observed to increase after treatment 

across treatment groups. WBC count was also significant (P < 0.05) in paired 

sample correlations across groups in 2nd and 3rd studies respectively. 

 

Figure 3: RBC test results across groups. The RBC values for the baseline 

study, the post induction study (2nd study) and post treatment study (3rd study) 

were distinguished. RBC values was reduced in the post induction study (2nd 

study) and increased at the treatment study across treatment groups (B, C & D) 

in comparison to lead only (E) group, which registered steady decline in RBC 

values. Paired sample correlates across groups in 2nd study and 3rd study 

groups also showed no significant difference (P > 0.05). 

A B C D E

Baseline 9.3 8.1 7.43 7.3 9.33

PIS 9.33 4 4 3.966 5.3

Treatment 11.1 4.86 5.433 4.6 3.66

0
5

10
15

W
B

C
 C

O
U

N
T

GROUPS

WBC (X10)

Baseline PIS Treatment

A B C D E

Baseline 3.7 4.73 4.166 5.233 3.93

PIS 5.266 3.03 3.43 3.7 3.56

Treatment 5.8 4 4.433 4.8 2.233

0
1
2
3
4
5
6
7

R
B

C
 C

O
U

N
T

GROUPS

RBC (X12)

Baseline PIS Treatment



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

12 
 

 

Figure 4: The figure above shows HB test results across groups. The HB values 

for the baseline study, the post induction study (2nd study) and post treatment 

study (3rd study) were distinguished. Hemoglobin values was lower with 

continuous administration in group E (lead only group), in comparison to 

control group A and treatment group B, C and D. however, HB values was 

seen to reduce in the post induction study results and increase in the treatment 

study result across treatment groups. hemoglobin was significant (P < 0.05) in 

paired sample correlation across groups in post induction (2nd study) and post 

treatment (3rd study) groups. 

 

Figure 5: Platelets test results across groups. The platelets values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. Platelets values were continuously decreased in 

group E (Lead only) but there was no difference between treatment groups C, 

A B C D E

Baseline 16.366 19.96 15.36 17.16 18.33

PIS 20.4 10.6 11.56 11.23 12.96

Treatment 21.8 11.5 12.49 12.13 9.99

0
5

10
15
20
25
30

H
B

 C
O

U
N

T

GROUPS

HB (G/DL)

Baseline PIS Treatment

A B C D E

Baseline 261.33 230.33 245.66 250 270.33

PIS 267.66 173.66 170 183 163

Treatment 266 195.66 191.66 200.6 143

0
50

100
150
200
250
300
350

P
LA

TE
LE

TS
 C

O
U

N
T

GROUPS

PLATELETS (X10)

Baseline PIS Treatment



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

13 
 

D and B. Platelet values were reduced in post induction study and increased in 

treatment group across treatment groups in comparison to control group A. 

However, paired sample correlations were significant (P < 0.05) across groups. 

Biochemical: Antioxidant Evaluation 

 

Figure 6; Shows SOD test results across groups. The SOD values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. There was no significant difference (P> 0.05) in 

SOD values across all groups. Also consistent with paired sample correlation 

of 2nd and 3rd study. 

 

Figure 7; Shows MDA test results across groups. The MDA values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. In group E (lead only), MDA values increased 

at continuous induction of lead in comparison to control group A, treatment 

group B (lead and pyridoxine), C (lead and quercetin) and D (lead and ascorbic 

acid) where values were reduced after treatment. Values were significant at P< 

0.05 across groups. Also consistent with findings from paired sample 

correlation. 

1
1

.5
6

1
1

.6
3

1
0

.6
0

6

1
0

.4
4

1
1

.2
9

7
.7 9

.1
3

3

8
.9

6
6

7
.8

5
3

1
2

.9

1
2

.6
2

1
1 1
1

.0
4

1
1

.3
1

1
1

.8
3

A B C D E

GROUPS

SOD (U/L)

1st study 2nd study 3rd study

0
.5

1

0
.5

0
3

3

0
.3

8
3

3

0
.4

1
6

7

0
.1

7
6

0
.3

5

4
.5

5

4
.8

9

3
.6

7 4
.8

2
6

0
.2

9
3

3
.1

9 3
.8

3
3

3
.1

1
3

4
.8

7

A B C D E

GROUPS

MDA (MG/DL)

1st study 2nd study 3rd study



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

14 
 

 

Figure 8: Shows GSH test results across groups. The GSH values for the 

baseline study, the post induction study (2nd study) and post treatment study 

(3rd study) were distinguished. GSH values continuously decreased in lead only 

group (group E), while there was notable increase in GSH values of treatment 

groups. There was significant difference (P> 0.05) in GSH post treatment 

values when compared with results of the baseline studies across group. 

2
.6

6

4
.5

2
3

3
.4

2

2
.4

2
3

3
.3

74
.6

2
3

3

2
.5

2

3
.0

5

1
.7

6 2
.6

5

4
.7

4
.2

9

3
.9

2
.7

8
6

2
.4

5

A B C D E

GROUPS

GSH (MG/DL)

1st study 2nd study 3rd study



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

15 
 

Histomorphological analysis 

 

Figure 9; Sections of temporal cortices: (A) control rat (normal saline 

only)neuronal cells (arrow). cytoarchitecture appears normal. (B). Lead and 

Pyridoxine treated the cytoarchitecture appears normal with neuronal cells 

(arrow) (C) Lead  and Vitamin C the cytoarchitecture appears normal with 

neuronal cells (arrow)  (D) Lead and quercetin treated the cytoarchitecture 

appears normal with neuronal cells (arrow)  (E ) Lead only distortion of  the 

cytoarchitecture (arrow) with  mild glial cell infiltration. H&E. x200. 

Discussion  

Lead poisoning is known to cause iron deficiency which in turn is a strong 

contributing factor in the etiology of anemia (Staudinger & Roth, 1998). 

Anemia is classified as macrocytic, normocytic, or microcytic based on the size 

of red blood cells and the amount of hemoglobin (Sarma, 1990). A low level of 

hemoglobin reflects reduced PCV value, which is defined as the ratio of the 

RBC volume to the total blood volume (Beutler & Waalen, 2003). 

Additionally, anemia can be hypochromic when the MCHC value is low.In this 

study, lead toxicity was evident owing to the slightly decreased PCV and RBC 

values (Fig 1 & 3) across treatment groups. This is consistent with the findings 

of Mahdi et al., (2013) in a clinical study on lead-exposed workers. Also, 

WBC, HB, and Platelets count greatly decreased after induction of lead across 

all treatment groups (Fig 2, 4 & 5).This is consistent with the findings of 

previous studies (Omotayo et al.,2022; Mahdi et al., 2013; Nabil et al., 2012; 

Mugahi et al.,2003).  

Vitamin C was also observed to show curative effects by increasing PCV, 

RBC, WBC, HB and Platelets count after observed reduction by lead 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

16 
 

administration.This was attributed to its functional ability to donate reducing 

equivalents to prevent the formation of reactive oxygen that damage the RBC. 

This finding is in line with Ozor, (2020). In another study, ascorbic acid 

demonstrated a substantial rise in RBC, and WBC in ascorbic acid therapy 

(Masar et al., 2021). Pyridoxine also exhibited a similar effect as vitamin C on 

the PCV, RBC, WBC, HB, and Platelets counts. This is in line with the 

findings of Boleslaw et al., (2019). Quercetin enhanced all  the blood 

parameters evaluated: PCV, RBC, WBC, HB, and platelets count. This is 

suggestive of haematopoietic enhancing property and affirms reports 

supporting quercetin supplementation enhanced RBC, WBC HB, PCV and 

Platelets count (Yahaya et al., 2020; Kasmi et al., 2018; Keskin et al.,2016; 

Selvakumar et al., 2013; Mahmoud et al., 2013).  

Antioxidants play a vital role in mitigating the effect of oxidative stress on 

tissues and observations in this study showed SOD values after induction of 

lead were reduced but not significant across groups. Other studies have earlier 

reported similar outcomes (Jin et al., 2006; Ahmed et al., 2008). However, 

significant a increases in SOD activity has been reported in lead-exposed 

workers (Kasperczyk et al., 2009; Rendon-Ramirez et al., 2014). Lead toxicity 

level is evident as  an increased level of MDA recorded in this study. Thus is 

consistent with several studies which found MDA levels to be significantly 

higher in lead-exposed groups(Tenchova et al., 1997; Ye et al., 1999, 

Yucebilgiç et al., 2003, Gurer-Orhan et al., 2004, Kasperczyk et al., 2013, 

Oktem et al. 2004, Patil et al., 2006; Garçon et al., 2007; Ergurhan-Ilhan et al., 

2008;  Khan et al., 2008, Mohammad et al., 2008, Grover et al., 2010, 

Permpongpaiboon et al., 2011; Singh et al,, 2013). Further findings from this 

study also showed a significant decrease in GSH values on exposure to lead 

and several studies also identified a reduction in GSH levels in lead-exposed 

group (Mohammad et al., 2008; Feksa et al, 2012; Kasperczyk et al, 2013). 

However, few studies identified increased GSH levels in lead exposed group 

(Gurer-Orhan et al., 2004; Conterato et al., 2013). 

Evident from our findings quercetin considerably reduced MDA levels and 

increased SOD and GSH levels, thereby reaffirming its already described 

antioxidant properties (Yagmurca et al.,2015) and confirming the protective 

properties of Quercetin via the regulation of antioxidant and lip peroxidation 

entities (Polat et al., 2006; Ikizler et al., (2017). Vitamin C reduced lead-

induced oxidative stress by decreasing MDA levels while increasing SOD and 

GSH levels. Vitamin C has the tendency to ameliorate oxidative stress levels 

(Bailey et al., 2011; Ozor, 2021). Vollaard et al, (2005) also posited that 

Vitamin C supplementation decreased serum MDA in exercise-induced 

oxidative stress. Pyridoxine also improved antioxidant markers. Pyridoxine 

supplementation exerted antioxidant and lipid profiles oflead-induced 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

17 
 

neurotoxicity (Tas et al., 2017).  

Histological observations revealed normal cytoarchitecture of the temporal 

cortices of the treated groups but not lead which revealed mild glial 

infiltrations. This was attributed to the lead effect on the cortex.Lead acetate 

caused mild histomorphological alterations in the brain (Jarrar et al., 2012) and 

dose- dependant cellular degenerative changes (Highab et al., 2018). Thus, lead 

exhibited a neurotoxic effect while the treatment quercetin, vitamin C, and 

pyridoxine exerted neuroprotective potential. This result was consistent with 

previous studies which reported the protective and antioxidant roles of 

quercetin, vitamin C, and pyridoxine (Vollard et al, 2005; Ikizler et al, 2017; 

Amanda et al, 2019; Ozor, 2021). Quercetin, particularly, enhances the 

survival of neuronal cells in the cerebral cortex (Khan et al, 2018). 

Conclusion 

Lead-induced oxidative stress consequently altered hematological parameters 

and temporal cerebral microstructure. The treatments with quercetin, ascorbic 

acid, and pyridoxine mitigated the adverse effect of lead via hematopoietic, 

antioxidant, and neuroprotective mechanisms. 

Conflict of Interest 

The authors declared that the research was conducted in the absence of any 

commercial or financial relationship that could be construed as a potential 

conflict of interest.  

Acknowledgement 

We thank the staff of the histology laboratory for providing the technical 

assistance. 

Author Contributions 

FBE: conception and design and supervised the research; MEC: wrote the 

draft; assembled and analyzed the histology; NIS and VU: performed the study, 

contributed to the discussion, reviewed; OII: review literature and edited the 

draft. All authors read and approved the manuscript. 

 

References  

Adonaylo, A., and P. Oteiza (1999). Lead intoxication: Antioxidant and 

oxidative damage in rat brain. Toxicology. 135: 77.  

Al-kurdy, M. (2021). Effect of ascorbic acid supplement on hematological 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

18 
 

parameters and some enzyme activities of Male Rabbits. Annals of the 

Romanian society for cell biology. 25.2758-2764. 

Amanda, D., Giustina, F, P. (2019). Vitamin B6 reduces oxidative stress in 

lungs and liver in experimental sepsis. Biological Sciences. An. Acad. Bras. 

Ciênc. 91 (04); https://doi.org/10.1590/0001-3765201920190434 

Bailey, C D. M., Williams, J. A., Betts, D., Thompson, T. L. (2011). Oxidative 

stress, inflammation and recovery of muscle function after damaging exercise: 

effect of 6-week mixed antioxidant supplementation. European Journal of 

Applied Physiology, vol. 111, no. 6, pp. 925–936, 

Bellinger, D.C. (2004). Lead. Pediatrics.113:1016–1022. 

Beutler, E., Waalen, J. (2006). The definition of anemia: what is the lower limit 

of normal of the blood hemoglobin concentration? Blood.;107(5):1747–50. 

Brent, J.A. (2006). Review ofMedical Toxicology. Clin Toxicol.;44:355–355. 

Conterato, G.M., Bulcao, R.P., Sobieski, R., Moro, A.M., Charao, M.F., de 

Freitas, F.A.,et al. (2013). Blood thioredoxin reductase activity, oxidative stress 

and hematological parameters in painters and battery workers: relationship 

with lead and cadmium levels in blood. J Appl Toxicol 33(2):142–150. 

doi:10.1002/jat.1731 

Ergurhan-Ilhan, I., Cadir, B., Koyuncu-Arslan, M., Arslan, C., Gultepe, F.M., 

Ozkan, G. (2008) Level of oxidative stress and damage in erythrocytes in 

apprentices indirectly exposed to lead. Pediatr Int 50:45-50 

Feksa, L.R., Oliveira, E., Trombini, T., Luchese, M., Bisi, S., Linden, R.,et al. 

(2012). Pyruvate kinase activity and delta-aminolevulinic acid dehydratase 

activity as biomarkers of toxicity in workers exposed to lead. Arch Environ 

Contam Toxicol 63(3):453–460. doi:10.1007/ s00244-012-9786-z 

Flora, S.J., Flora, G, Saxena, G. Mishra,, M. (2007). Arsenic and lead induced 

free radical generation and their reversibility following chelation. Cell Mol 

Biol (Noisy-le-grand);53:26–47.  

Flora, S.J.S. (2002). Nutritional components modify metal absorption, toxic 

response and chelation therapy. J Nut Environ Med.;12:53–67. 

Formica, J.V., Regelson, W. (1995). Review of biology of Quercetin and 

Related Bioflavonoids. Food and Chemical Toxicology, 33, 1061-1080. 

http://dx.doi.org/10.1016/0278-6915(95)00077-1 

Garçon, G., Leleu, B., Marez, T., Zerimech, F., Haguenoer, J.M., Furon, D., 

Shirali, P. (2007). Biomonitoring of the adverse effects induced by the chronic 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

19 
 

exposure to lead and cadmium on kidney function: Usefulness of alpha-

glutathione S -transferase. Sci Total Environ 377:165–172 

Ghanwat, G., Patil, A.J., Patil, J., Kshirsagar, M., Sontakke, A., Ayachit, R.K.. 

(2016). Effect of Vitamin C Supplementation on Blood Lead Level, Oxidative 

Stress and Antioxidant Status of Battery Manufacturing Workers of Western 

Maharashtra, India. J Clin Diagn Res. Apr;10(4):BC08-11. doi: 

10.7860/JCDR/2016/15968.7528. 

Grover, P., Rekhadevi, P.V., Danadevi, K., Vuyyuri, S.B., Mahboob, M., 

Rahman, M.F. (2010). Genotoxicity evaluation in workers occupationally 

exposed to lead. Int J Hyg Environ Health 213:99–106 

Gurer-Orhan, H., Sabir, H.U., Ozgunes, H. (2004). Correlation between 

clinical biomarkers of lead poisoning and oxidative stress parameters in 

controls and lead-exposed workers. Toxicology 195:147–154 

Highab, S.M., Magaji, R.A., Muhammad, B.Y. (2018). Effects of lead 

poisoning and antidepressant drugs on the cerebral cortex of Wistar rats. Acta 

Scientific Pharmaceutical Sciences 2.5.16-21. 

Hsu, P.,  Guo Y (2002). Antioxidant nutrients and lead toxicity. Toxicology 

180: 33–44 

Ikizler, M., Erkasap, N., Dernek, S., Kural, T., Kaygisiz, Z. (2007). Dietary 

polyphenol quercetin protects rat hearts during reperfusion: enhanced 

antioxidant capacity with chronic treatment. Anadolu Kardiyol Derg; 7 (4): 

404–410. 

Jarrar, B.M., Taib, N.T. (2012). Histological and histochemical alterations in 

the liver induced by lead chronic toxicity. Saudi J Biol Sci. Apr;19(2):203-10. 

doi: 10.1016/j.sjbs.2011.12.005.  

Jin, Y., Liaob, Y., Lua, C., Lia, G., Yue, F., Zhic, X., Xud, J., Liud, M., Yang, 

J., (2006). Health effects in children aged 3-6 years induced by environmental 

lead exposure. Ecotoxicol Environ Saf 63:313-317. 

Kalicki, B., Aneta, L., Krystyna, J., Monika, L., Justyna, M.J., Slawomir, L. 

(2019). Vitamin B6 improves blood parameters in rats fed a protein deficient 

diet and subjected to moderate, long term exercise. Cent Eur J Immunol. 

44(1):23-32. 

Kasmi, S., Bkhairia, I., Harrabi, B., Mnif, H., Marrakchi, R., Ghozzi, H., et 

al.(2018). Modulatory effects of quercetin on liver histopathological, 

biochemical, hematological, oxidative stress and DNA alterations in rats 

exposed to graded doses of score 250. Toxicol Mech Methods ;28:12-22 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

20 
 

Kasperczyk, S., Kasperczyk, J., Ostalowska, A., Zalejska-Fiolka, J., 

Wielkoszynski, T., Swietochowska, E., Birkner, E. (2009). The role of the 

antioxidant enzymes in erythrocytes in the development of arterial 

hypertension among humans exposed to lead. Biol Trace Elem Res 130:95–106 

Kasperczyk, S., Slowinska-Lozynska, L., Kasperczyk, A., Wielkoszynski, T., 

Birkner, E. (2013). The effect of occupational lead exposure on lipid 

peroxidation, protein carbonylation, and plasma viscosity. Toxicol Ind Health. 

doi:10.1177/0748233713491804 

Keskin, E., Dönmez, N., Kılıçarslan, G., Kandır, S. (2016). Beneficial effect of 

quercetin on some haematological parameters in streptozotocin-induced 

diabetic rats. Bull Environ Pharmacol Life Sci 2016;5:65-8. 

Khan, D.A., Qayyum, S., Saleem, S., Khan, F.A. (2008). Lead-induced 

oxidative stress adversely affects health of the occupational workers. Toxicol 

Ind Health 24:611–618 

Kuhad, A., and Chopra, K. (2007). Curcumin attenuates diabetic 

encephalopathy in rat: Behavioral and biochemical evidence. European Journal 

of Pain 576: 34. 

Mahmoud, A.M. (2013). Hematological alterations in diabetic rats - Role of 

adipocytokines and effect of citrus flavonoids. EXCLI J;12:647-57. 

Mohammad, I.K., Mahdi, A.A., Raviraja, A., Najmul, I., Iqbal, A., Thuppil, V. 

(2008) Oxidative stress in.painters exposed to low lead levels. Arh Hig Rada 

Toksikol 59:161–169 

Monteiro, H.P., Abdalla, D.S.P., Arcuri, A.S., Bechara, E.J.H. (1985) Oxygen 

toxicity related to exposure to lead. Clin Chen 31(10):1673–1676 

Mugahi, M.N., Heidari, Z., Sagheb, H.M., Barbarestani, M. (2003). Effects of 

chronic lead acetate intoxication on blood indicies of male adult rat. DARU 

Journal of Pharmaceutical Sciences 11(4):147-151. 

Nabil, M.I., Esam, A.E., Hossam S.E., Yasmin, E.A.M. (2012). Effect of lead 

acetate toxicity on experimental male albino rat. Asian Pac J Trop Biomed 

Jan;2(1):41-46. 

Oktem, F., Arslan, M.K., Dündar, B., Delibas, N., Gültepe, M., Ergürhan-

Ilhan, I. (2004). Renal effects and erythrocyte oxidative stress in long-term 

low-level lead-exposed adolescent workers in auto repair workshops. Arch 

Toxicol 78:681–687 

Omotayo, B.1., Esther, F.A., Temitope, T.O., Bruno, C. (2022). Lead exposure 

– induced changes in hematology and biomarkers of hepatic injury: protective 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

21 
 

role of Trevo supplement. Environ Anal Health Toxicol; 37(2):e2022007. 

Ozor, I.I. (2021). Biomarker patterns and neuroprotective effects of ascorbic 

acid, progesterone and statin in induced traumatic brain injury using a rat 

model. Apr, 

Patil, A.J., Bhagwat, V.R., Patil, J.A., Dongree, N.N., Ambekar, J.G., Das, 

K.K. (2006). Biochemical aspects of lead exposure in silver jewelry workers in 

Western Maharashtra (India). J Basic Clin Physiol Pharmacol 17(4):213–229. 

Permpongpaiboon, T., Nagila, A., Pidetcha, P., Tuangmungsakulchai, K., 

Tantrarongroj, S., Porntadavity, S. (2011). Decreased paraoxonase I activity 

and increased oxidative stress in low lead - exposed workers. Hum Exp 

Toxicol 30(9):1196–1203. 

Polat, C., Tokyol, C., Kahraman, A., Sabuncuoglu, B., Yilmaz, S. (2006). The 

effects of desferrioxamine and quercetin on hepatic ischemia-reperfusion 

induced renal disturbance. Prostaglandins Leukot Essent Fatty Acids; 74 (6): 

379–383. 

Raymond, F. (2011). Lead presentation on biology 464 aquatic toxicology 

Razmkon,, A., Sadidi, A., Sherafat-Kazemzadeh, E., Mehrafshan, A., Jamali, 

M., Malekpour, B., Saghafinia, M. (2011) Administration of vitamin C and E 

in sever head injury: a randomized double-blind controlled trial. Clin 

Neurosurg; 58:133-7. Doi: 10.1227/nue.0bo13e3182279a8f.PMID:21916138. 

Rendon-Ramirez, A.L., Maldonado-Vega, M., Quintanar-Escorza, M.A., 

Hernandez, G., Arevalo-Rivas, B.I., Zentella-Dehesa, A., Calderon-Salinas, 

J.V.M. (2014). Effect of vitamin E and C supplementation on oxidative 

damage and total antioxidant capacity in lead-exposed workers. Environ 

Toxicol Pharmacol 37(1):45–54. doi:10.1016/j.etap.2013.10.016 

Roels, H.A., Buchet, J.P., Lauwerys, R.R., Sonnet, J. (1975). Comparison of in 

vivo effect of inorganic lead and cadmium on glutathione reductase system and 

δ-aminolevulinate dehydratase in human erythrocytes. Br J Ind Med 32:181–

192 

Sarma ,P.R. (1990). Red cell indices. Clinical methods: The history, physical, 

and laboratory examinations. 3rd ed. Butterworths;. 

Selvakumar, K., Bavithra, S., Suganya, S., Ahmad, B.F, Krishnamoorthy, G., 

Arunakaran, J. (2013). Effect of quercetin on haematobiochemical and 

histological changes in the liver of polychlorined biphenyls-induced adult male 

Wistar rats. J Biomark:960125. 

Sina, K., Mahdi, B.M., Seyed, R.M., Mohammad, T.S., Bita, D., Valiollah, M., 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

22 
 

Mahmoud, S. (2013). Clinical, Toxicological, biochemical and hematologic 

parameters in lead exposed workers of a car battery industry. Iran J Med Sci. 

Mar;38(1):30-37. 

Singh, Z., Chadha, P., Sharma, S. (2013). Evaluation of oxidative stress and 

genotoxicity in battery manufacturing workers occupationally exposed to lead. 

Toxicol Int 20(1):95–100. doi:10.4103/0971-6580.111550 

Sriraksa, N., Wattanathorn, J., Muchimapura, S., Tiamkao, S., Brown, K., 

Chaisiwamongkol, K. (2012). Cognitive-enhancing effect of quercetin in a rat 

model of Parkinson’s disease induced by 6-hydroxydopamine. Evid Based 

Complement Alternt. Med.:823206 

Staudinger, K.C., Roth, V.S. (1998). Occupational lead poisoning. American 

family physician, 57, 719-726. 

Syeda, M., Zehra, B., Saiqa, T., Laraib, L., Sadia, S., Sidrah, S., Fizza, N., 

Sadia, S., Sarwat, Y., Amber, N., Saara, A., Irfan, S., Asia, A., Saida, H. 

(2021). Quercetin exhibits potent antioxidant activity, restores motor and non-

motor deficits induced by rotenone toxicity; 

https://doi.org/10.1371/journal.pone.0258928 

Taş, S., Sarandöl, E., Dirican, M. (2014). Vitamin B6 supplementation 

improves oxidative stress and enhances serum paraoxonase/arylesterase 

activities in streptozotocin-induced diabetic rats. Scientific World 

Journal.;2014:351598. doi: 10.1155/2014/351598. 

Tenchova, V., Petkova, V., Pavlova, S., Simeonov, I. (1997). Lipid 

peroxidation in chronic lead exposure. Probl Khig. 22:54–61 

Todorova, I., Simeonova, G., Kyuchukova, D. (2005). Reference values of 

oxidative stress parameters (MDA, SOD, CAT) in dogs and cats. Comp Clin 

Path13, 190-194. 

Vollaard, N. B. J., Shearman, J. P., Cooper, C. E. (2005). “Exercise-induced 

oxidative stress: myths, realities and physiological relevance,” Sports 

Medicine, vol. 35, no. 12, pp. 1045–1062, 

Yagmurca, M., Yassar, Z., Bas, O. (2015). Effects of quercetin on kidney 

injury induced by doxorubicin. Bratisl med.j, 116(8). Doi: 10.4149/BLL-092. 

Yahya, P., Farhad, O., Mahin, N.Z., Mehrnaz, A., Azizollah, P., Mahboobe, H. 

(2020). Effects of Quercetin Supplementation on Hematological Parameters in 

Non-Alcoholic Fatty Liver Disease: a Randomized, Double-Blind, Placebo-

Controlled Pilot Study. Clin Nutr Res.Jan;9(1):11-19 

Ye, X., Fu, H., Zhu, J., Ni, W., Lu, Y., Kuang, X., Yang, S., Shu, B. (1999). A 



Global Online Journal of Academic Research (GOJAR), Vol. 2, No. 1, Jan-Feb 2023 

 

 

23 
 

study on oxidative stress in lead-exposed workers. J Toxicol Environ Health A 

56:161–172 

Yucebilgiç, G., Bilgin, R., Tamer, L., Tukel, S. (2003). Effects of lead on Na + 

-K + ATPase and Ca +2 ATPase activities and lipid peroxidation in blood of 

workers. Int J Toxicol 22:95–97 

 

 

Author Information: Nnachi Ifenna Salvator is of the Department of 

Anatomy, Faculty of Basic Medical Sciences, Enugu State University of 

Science and Technology, Parklane, Enugu State, Nigeria. Email 

(correspondence author): nnachiifenna@gmail.com  
 

 

Dr (Mrs) Elizabeth Finbarrs-Bello is a lecturer at the Department of 

Anatomy, Faculty of Basic Medical Sciences, Enugu State University of 

Science and Technology, Parklane, Enugu State, Nigeria. Email: 

elizabeth.finbarrs-bello@esut.edu.ng 

 

 

Ozor Ignatius Ikemefuna is of the Department of Anatomy, Faculty of 

Basic Medical Sciences, Enugu State University of Science and 

Technology, Parklane, Enugu State, Nigeria. 

 

 

Mba Christian Ejuiwa is affiliated to the Department of Anatomy, Faculty 

of Basic Medical Sciences, Enugu State University of Science and 

Technology, Parklane, Enugu State, Nigeria. 

 

 

Vivian Ugwu is affiliated to the Department of Anatomy, Faculty of Basic 

Medical Sciences, Enugu State University of Science and Technology, 

Parklane, Enugu State, Nigeria. 

 

 

 

 

 

 

 

 

 

 

 

 


