IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 Lipid Peroxidation, Prooxidant and Related Antioxidant Proteins in Various Types of Hyperlipoproteinemic Males and Control W.F.Al-Tai Departme nt of Chemistry ,College of Education I bn-Al-Haitham, Unive rsity of Baghdad Abstract Thirty nine hy p erlipop roteinemic (HPLic) male subject aged (48-63) y ear not on any of the lip id lowering drugs, att ending out p atient clinic at Baghdad Teaching Hosp ital, were included in the p resent st udy , in addition to twenty two normolipidimic male subjects of matched age were included as control throughout this st udy . The first p art of this st udy was devoted to the classification of the HPLic subjects according to the serum lip id and lip op rotein p rofile following defined criteria. The lip id p arameter including total cholesterol (TC), triglyceride (TG), high density lip op rotein (HDL) and low density lip op rotein (LDL) were invest igated in serum of HPLic subjects included in the st udy . The classification was p erformed according to Frederickson's ty p e, as t wenty one hyp ercholest erlemic (ty p e IIa), and eighteen hy p ertriglycerdimia (ty p e IV) HPLic subjects. In the second p art of the st udy , lip id p eroxidation marker measured as malondialdehyde (M DA), free iron, ferritin, transrerrin (Tf) and ceruloplasmin (Cp) levels were measured in the serum of all subjects included in the study . The results indicated that significant increase was observed in the serum levels of Tc, Tg and LDL in ty p e IIa and Ty p e IV HPLic comp ared to control, and a significant decrease in HDL level in serum of both HPLic group comp ared to control, while no significant difference in serum HDL levels between ty p e IIa and ty p e IV HPLic was found. The mean M DA, free iron and ferritin levels in serum were found to be significantly higher in both ty p es IIa and IV HPLic compared to control, also ferritin level in serum of ty p e IV showed a significant increase over that of ty p e IIa (257.3±22.7 vs. 223±19.2 mg/ml; p <0.05). On the other hand, no significant difference in mean M DA and free iron levels between both ty p es of HPLic group s were found. The mean Tf and Cp levels in serum of ty p e IIa HPLic group showed a slight increase, y et not significant when comp ared to control, but a non significant decrease in Tf and Cp levels in serum of ty p e IV HPLic group comp ared to control was found, however neither Tf nor Cp levels showed any significant difference between both HPLic group s. These results suggest the presence of oxidative st ress injury in subjects with either ty p e IIa or IV HPL, which could be due to high levels of LDL which is more susp tible to oxidation and high levels of serum free iron which act as a p rooxidant agent in its free form. Introduction A series of cytotoxic oxy gen sp ecies p lay s an imp ortant role in various disease as associated with dy slipidemia causing cell damage including lip id p eroxidation, inactivation of enzy mes, alteration of intracellular oxidation-reduction st ate and damage to DNA[1, 2] Lip op roteins are essential for the transp ortation of lip ids in the vascular sy st em. Inherited defects in lip op rotein metabolism lead to the p rimary condition of either hy p o or hy p er lip op roteinemia (HLP), a few individuals in the p op ulation exhibit inherited defects in their lip op roteins leading to the p rimary condition. In addition, diseases such as diabetes mellitus, hy p othy rodism and coronary heart diseases are associated with secondary abnormal IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 lip op rotein p att erns that are very similar to one or another of the p rimary conditions. Virtually ,all the p rimary conditions are due to defect at a st age in lip op rotein formation, transp ort or destruction, however not all of the abnormalities are harmful[3, 4]. Iron p lay an imp ortant role in many biological p rocesses because it is an ideal O2 carrier and it is an essential cofactor for numorous iron containing comp ounds, in form of heme or noheme st ructure to limit the availability of free iron which contribute to free radical p roduction via cataly zing Haber-Weiss and Fenton reaction[5]. Iron is taken-up by intest inal mucosa as Fe++ and converted to the trivalent form which bound to transferrin (Tf), aglycoprotein with two iron-binding sites, which transp orts iron to the liver or sp leen where the fraction of unused and highly toxic iron is st ored as ferritin molecules in order to be neutralized. A p oferrintin, the p rotein fraction of ferritin, is sp atially folded to create a central groove that holds oxidized iron molecules, the heavy chain in apoferritin molecule exerts ferroxidase activity , cataly zing the oxidation of ferrous to ferric ions, which p revents iron- induced cyclic redox reactions that would sp read and amp lify the oxidative damage to living cells. This activity occurs under aerobic conditions, allowing the st orage of intracellular iron[6,7]. However cerulop lasmin (CP) (the copp er carrying p rotein) seems to p lay a key role in the oxidation of ferrous iron and hence it releases from cells and loading onto apotransferrin, as the transferring binds largely the ferric form, so Cp is involved p rimarily in maintaining iron homeost asis and p reventing iron-mediated free radicals injury , thus Cp is considered as antioxidant through its ferroxidase activity [8]. Hy p erlipop roteinemia could increase levels of oxy gen free radicals in various way s; hy p ercholest erolemia increases cholesterol content of p latelets, p olymorphonucleare leukocytes and endothelial and smooth muscle cells, neutrop hils, nonocy tes, and platelets may be the source of oxy gen free radicals in hyp ercholest erolemia[9]. Ant ioxidant substance are used to keep free radicals under or at p hy siological control levels [10]. However, in the literature there were limited and conflicting data on the relationship between lip id p eroxidation, iron as aprooxidant agents and some related p roteins as antioxidant. Therefore this study was carried out t o exp lore whether important p roteins of iron metabolism are altered in subjects with various ty p e of HPL, namely the ferritin, tansferrin, and cerulopasmin, since binding of iron to these p roteins p revents, or greatly decreases p articip ation of this metal in oxy gen radical formation. Experimental Part S ubjects The p resent st udy was p erformed on males aged 48-67 y ears with different lip op rotein p rofile attending out p atient clinic at Baghdad Teaching Hosp ital. Noromolip idemic subjects were recurred from male subjects aged 45-65 y ears, who had p lasma triglyceridws (TG)<203 mg/dl and total cholesterol (Ch)<217 mg/dl, according to criteria in Tietz (1999)[11]. No medication known to influence the lip id st atus was admistrated in any of the subjects during the last six months. Patients with diabetes mellitus, hy p othy rodism, nephritic sy ndrome or any other serious illness during the pervious six months were excluded. The classification of HPLic subjects was made according to Fredrickson's ty p e, as following criteria in (Tietz 1999) [11] Ty p e IIa HPL: p lasma TG<203 mg/dl, total Ch>270 mg/dl and LDLc>131 mg/dl. Ty p e IV HPL: p lasma TG>203 mg/dl, total Ch<270 mg/dl and LDLc<131mg/dl. Blood was drawn from subjects fasting (>12 hours) with t y p e IIa (n=21), ty p e IV (n=18) HLP and an age matched normolipidimic as control group (n=22). IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 In p lain tubes 5ml blood was left to clot at room temp erature for 15 minutes, centrifuged at 3500 rp m to separate serum from erythrocytes. Sera were used directly for some p arameter measurements; the rest was divided in to small p ortions and kep t frozen. Lipid profil e anal ysi s Fraction of serum lip ids was p erformed by using ready kit from Bio M erieux A.S., France as follows: Serum total Ch was determined by the Ch enzy matic method using a series of enzy mes (i.e. Ch east erase, Ch oxidase and p eroxidase). The chromagnic comp elex formed was followed colorimetrically at soon, the absorbance of a known concentration of st andard Ch was used to determine the concentrations of samp les by p rop ortion[12]. 1- Serum TG was determined colorimetrically by TG enzy matic method using a series of enzy mes (i.e. lip ase, glycerokinase, glycerol-3-phosp hate oxidase and p eroxidase)[13]. 2- Serum LDLc was estimated indirectly by the use of Friedewald FormulaSerum HDLc was determined after p recipitation of chylomicron, VLDL and LDL contained in the serum samples by the addition of 4% p hosp hotungst ic acid solution magnesium chloride, the sup ernatant obt ained after centrifugation contains the HDL, from which the Ch was determined as described in [12]. Lipid peroxidation marker determination M alondialdehy de (M DA), an end p roduct of the breakdown of p olyunsaturated fatt y acids, reacts with thiobarbituric acid to give a red chromop hor that has a maximum absorbance at 532 nm. In this method, p rotein was p recipitated with trichloroacetic acid (70%) which also acidifies t he medium; chloroform was added to remove the disp ersed lip ids then centrifuged. The absorbance of the sup ernatant was recorded at 532 nm against a blank. The M DA concentration was calculated by using molar absorbtivity coefficient of 1.56×105 L.mol-1.cm-1 [15]. S erum iron determination The iron was determined in the serum by using a ready kit from TECO Diagnost ics France. The iron is allowed to dissociate from its ferric transferrin comp lex by the addition of an acid buffer containing hy droxy lamine. This p rocess reduces the ferric iron to ferrous form. The chromogenic agent (i.e. Ferene) p rovided with the kit, will form a highly colored ferrous comp lex, which is measured sp ectrop hotometrically at 560nm. Transfe rring (Tf) dete rminatiom The concentration of the Tf was determined indirectly as the ability of p lasma p rotein to bind iron, the so called total iron-binding cap acity (TIBC), where the unsaturated iron binding cap acity (UIBC) is determined by the addition of a known ferrous salt concentration to the serum samp le, so the added iron will bind to the unsaturated sites on transferrin. The excess (unbound) iron are reacted with ferene to form the colored comp lex and determined as in the method of serum iron determination using the ready kit TECO Dignost ic France. The difference between the added iron and the amount of iron measured represents the unsaturated iron binding cap acity ; therefore the (TIBC) is determined by adding the serum iron value to the UIBC value. Then transferrin was est imated from the following equation[16]: Transferring (mg/dl) = 0.7×T IBC (mg/dl). Ferriti n dete rmination Ferritin concentration in serum was determined by using a human ferritin test kit sup p lied by Bio Check Company U.K. The method based on solid p hase enzy me linked immunosorbent assay (ELISA), where a sy st em utilizes one rabbit anti-ferritin antibody for IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 the solid p hase (microtiter wells) immobilization and a mouse monochlonal anti-ferritin antibody for the solid p hase (microtiter wells) immobilization and a mouse monochlonal anti- ferritin antibody in the antibody -enzy me (horseradish p eroxidase) conjugate solution[17]. Ce rulopasmi n (Cp) determination The method for Cp concentration in serum based on the cataly tic ability of Cp to oxidize the colorless P-p henylene diamine to a blue –violet oxidize form which has maximum absorbent at 525nm, using molar absorbtivity coefficient of 0.68 mol-1.cm-1 for the base[18] . S tatisti cal analysi s The results were exp ressed as mean ±SD of mean, using st udents t-test, significant variation is considered when P-values is≤0.05. Re sults and Discussion Lip ids and lipop rotein p arameters in all subjects p articip ated in the st udy are shown in table (I). Control (normolip idemic),ty p e IIa HPL ( hy p ercholest erolemic ) and ty p e IV HPL (hy p ertriglyceridemic) were classified according to the criteria mentioned in the exp erimental p art (1). All lip id p arameters excep t for the high density lip op rotein (HDL) in both HPLic group s were significantly higher than of control group Excess Ch is p resent in the form of low density lip op rotein (LDL) p articles, so- called "bad Ch ", while the ratio of Ch in the form of (HDL), referred as "good Ch" to that in the form of LDL can be used to evaluate suscep tibility for the development of heart disease , due to the binding of HDL to the esterified Ch released from the p erip heral tissues and transfer cholestry l est ers to the liver or tissues t hat use Ch to sy nthesize st eroid hormones . T he exact nature of the p rotective effect of HDL levels is not known; however, a p ossible mechanism is that a serum esterase which degrades oxidized lip ids is found in association with HDL. Possibly ,the HDL-associated p rotein destroy s the oxidized LDL (ox-LDL), accounting for HDL's ability to p rotect against coronary diseases . On the otherhand oxidized atherogenic lip op rotein, namely ox-LDL is taken up by immune-sy st em cells (macrophages), which become engorged to foam cells. These foam cells would become trapp ed in the wall of the blood vessels and contribute to the formation of atherosclerosic p laques that cause arterial narrowing and lead to heart att acks [19]. The significant increase in serum LDL and the decrease in serum HDL in this st udy agree with results reported higher levels of LDL and lower levels of HDL in p lasma of HPLic subjects ,they also claimed that LDL p ossess a direct toxic effect on endothelial cells , and the p lasma concentration of ox-LDL might be one of the st rongest p redictors of endothelial dy sfunction in early atherosclerotic lesions [20]. It has been claimed that lower HDL values in p lasma of HPLic subjects is to counter balance the ox- LDL levels ,because HDL not only att ributed to maintain normal cell cholesterol homeost asis by the reverse Ch transp ort, but also p ossess considerable antioxidant p rop erties [21]. The results of lip id peroxidation marker M DA and free iron in serum of the three st udied group s are shown in table (II). A significant increase in M DA and free iron levels in the serum of both HPLic group s comp ared to control was found ,while no significant differences in the levels of both p arameters between both HPLic group s was noticed . The results of t he present st udy agree with others st udies reported higher plasma levels of M DA,ox-LDL and free iron in HPLic subjects , which was exp lained by the fact that the increased p lasma concentration of lip ids and lipop rotein (as substrate for oxidation ) results in higher concentration of their oxidation p roducts . It has been p ost ulated that HPL could IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 increase levels of oxy gen free radicals in various way s ; hy p ercholest erolemia increase Ch content of p lateles, leukocytes and endothelial cells so t hat endothelial , smooth muscle cells , neutrop hils and p latelets may be the source of oxy gen free radicals . It has been also demonst rated a higher oxidative st rees in HPLic subjects who also showed clinical sy mptoms of endothelial dy sfunction later indicating that ox-LDL p lay s the crucial role in early st ages of atherosclerosis [20,22,23] . Iron is intensively discussed as a p ossible risk factor of atherosclerosis, mainly for its cataly tic role in free radical formation and subsequent oxidative modification of atherogenic lip op rotein namely LDL [20]. On the otherhand a non –significant increase in p lasma free iron was reported in some subjects with HPL compared to control , y et an increased oxidative st ress markers were rep orted , which was claimed that an alteration in the antioxidant defence sy st em occur in resp onse to various diseases and HPL [24] . Increased iron availability is , theoretically , exp ected to contribute to macrovascular disease because iron has an adverse effect on endothelium , and accelerates the development of atherosclerosis through the oxidation of atherogenic lip op rotein , LDL [25] . Serum Tf, ferritin and Cp levels for ty p e IIa and ty p e IV HPLic group s with matched sex and age normolipidimic control are represented in table III. A significant increase in serum ferritin levels in both HPLic group s comp ared to control group was not iced. Similar results were rep orted, when analysing subjects with different ty p es of HPL. The authors stated that it is st ill unclear whether elevated iron st ores (ferritin) alone or p lasma free iron alone or both p lay a crutial role in p athogenesis for atherosclerosis and cardiovascular risk developing in such subjects [20]. However , a p ossible exp lanation for the relation between serum free iron and ferritin comes from the fact that sy nthesis of apoferritin is induced at both the transcrip tional and p ost transcrip tional levels by the presence of free iron , since iron can be released from ferritin by the action of many factors including reducing agent t hat convert ferric to ferrous forms , so the increase in the ferrous form downregulates the affinity of iron-regulatory element (IRE ) binding p rotein (BP) for its IRE binding site in the s region of ferritin mRNA , leading to increase ferritin translation , also when the concentration of antioxidants are low ,the reducing p otential and anaerobiosis p rogressively increase , facilitating a rapid release of iron from ferritin . Additionaly, the ferroxidase activity in the heavy chain of apoferritin is downregulated in this setting, decreasing the incorp oration of iron into ferritin. The overall result of oxidative reactions is an increase in the availability of free iron from ferritin molecule as well as from other molecules (containing iron) undergoing degradation. These events, in turn, can enhance and amp lify the p rocess of generation of free radicals, causing cellular and tissue damage .The oxidative st ress also downregulates the affinity of IRE for IRE-Bp. Thus, ferritin can act both as a source of iron , which induce oxidative st ress , and as a mechanism that p rotects against the formation of highly toxic free radicals , which are cap aple of inducing lip id peroxidation [26,27,28]. The levels of TF and Cp in serum of both HPLic subject group s were not significantly alterd from that of control group , thus the results of the p resent st udy agreed p artly with a st udy reported a significant increase in p lasma Cp levels and non significant differences in p lasma Tf levels of HPLic subjects t hey also reported that the increase of Cp level was more p ronounced in HPLic subjects with diabetes , due to the consideration of Cp is one of the p ositive acute –phase reactants , whose concentration increase up on different diseases and this increase come from an increase liver sy nthesis of Cp through the enhancement of ceruloplasmin mRNA transcrip tion and/or a decrease in catabolism of this p rotein [29]. The results of the present study agree with reported data stated that neither Tf nor Cp in plasma of HPLic showed significant differences from that for normolipidemic subjects [22] . Two imp ortant agents were reported to be resp onsible for extracelluar antioxidant activity , through their rotes in iron homostasis, these are the copp er containing p rotein , Cp and the iron-binding p rotein Tf , as Cp convert reduced iron released from its st orage site (ferritin )to t he oxidized form by this way Cp allows iron to bind to its p lasma transp orter IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 p rotein (transferrin), while Tf carries iron to st orage site , at this site , the iron is released from Tf and st ored inside cells as ferritin, then Tf may be used again for further iron transp ort [30,31]. In conclusion, this st udy shows t hat both subjects with either ty p e IIa or ty p e IV HPL have enhanced lip id p eroxidation in their serum. The elevated serum LDL concentration, which is more susp tible to oxidation, in addition to high serum iron levels, may result in higher lip id p eroxidation . However the decreased concentration of HDL and non-increased levels of Cp and Tf as antioxidant are not likely to be sufficient enough to counter higher reactive oxy gen metabolites p roduction in HPLic subjects, which may cause oxidative st ress leading to cellular and molecular damages thereby resulting in development of cardiovascular diseases. Therefore further st udies needed to clarify the relation between lip id p eroxidation and other antioxidant p arameters of the defense sy st em to draw a conclusion as to whether the changes in this antioxidant are causes or results of increased oxidative st ress. Re ferences 1.Taysi,S.; Gul,M .; Saru,R.A.; Akcay ,F. and Bakan,N., (2002) : Clin. Chem. Lab. M ed.; 40: 684-688. 2.Prashant, A.V.;Harishchandra, H.; Dsouz a, V. and Dsouz a, B., (2007) : Indian Journal of Clinical Biochem.; 22(1): 131-134. 3.M urray, R.K.; Granner, D.K. and Rodwell, V.W., (2006): "Harp p r's Illustrated Biochemistry " 27 th Edition, Lange M edical Books, M c Graw- Hill comp anies U.S.A.; p 239. 4.Bishop , M .L.; Fody , E.P. and Schoeff, L., (2005) "Clinical Chemist ry " 5 th Edition, Lip p incott Williams and Wilkins, A Wolters Kluwer Kluwer Comp any, Philadelp hia; p p .293-298. 5.Finch, C. (1994): Blood; 84:1697-1702. 6.Hubers, H.A. and Finch, C.A., (1987): Phy siol Rev. 67:250-282. 7.Jukell, M .B.; Balla, J.; Jessurun, J. and Vercellott , G.M ., (1995): Am. J. Pathol; 147:782- 789. 8.Richardson, D.R., (1999): J. Lap. Clin. M ed; 134: 454-465. 9.Esterbauer, H.; Gebicki, J.; Puhl, H. and Jurgens, G., (1992): Free Radical Biol. M ed.; 13:341-390. 10.Dip lock, A.T .; Charleux, J.L.;Crozier-Willi, G. and Ricevance,C., (1998): British Journal of Nut rition; 80.81-96. 11.Tietz, N.W., (1999): "Textbook of Clinical Chemistry ", WB Saunders Comp any, Philadelp hia, p p 809-861. 12.Richmond, W., (1974): Clin. Sci. M ol. M ed.; 46: 6-7. 13.Fsssati, P. and Prencip e, L., (1982): Clin. Chem., 28(10): 2077-2080. 14.Friedewald, W.T.; Levy, R.I. and Fredrickson, D.S., (1972); Clin Chem, 18:499-502. 15.Fong, K.L.;M c Cay , P.B. and Poy er, J.L., (1973): J. Biol. Chem.; 248:7792-7797. 16.Burtis, C.A. and Ashwood, E.R. (1996): "Tetiz Fundamentals of Clinical Chemistry " Eds. Philadelp hia, Sunders WB Fourthed 309. 17.White, D.M .;Kramer, D.; Johnson, G.; Dick, F. and Hamilton, H. (1986): Am. J. Ciln. Path; 72: 346-349. 18.M enden, C.E.; Boian, J.M .; M urthy , L. and Petering, H.G., (1977): Anal Lett; 10:197-204. 19.Berg, J.M .;Ty moczko, J.L. and Stry er, L., (2007): "Biochemist ry " 5 th ed. W.H. Freeman and Comp any, New York. 20.Kraml, P., Syrovaka, P., Stip ek, S., Fialova, L. and Andel, M ., (2004): Phy siol. Res.; 53: 471-480. 21.Hsueh,W.A. and Quinonws, M .J., (2003): Am. J. Cardiol; 92:10-17. 22.Efe, H.; Kirci, D.;Deger, O. and Orem, C. (2004): Tohoku. J. Exp . M ed.; 202: 163-172. IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 23.Dave, G.V. and Kalia, K., (2007): Cell M ol Bio; 53:68-78. 24.Godin, D.V. and Dahlman, D.M ., (1993): Res. Commun. Chem. Pathol Phamacol; 79:151- 166. 25.Tuomainen, T.P.; Punnonen, K. and Salonen, J.P., ()1998 : Circulation; 97:1461-1466. 26.Reif, D.W., (1992): free radi Biol M ed; 12: 417-42 27.Juckett ,M .B.; Balla, J.; Jessurun, J. and Jacob, H.S., (1995): Am. J. Pathol.; 147: 782-789. 28.Fernandez-Real, J.M .; Bermejo, A.L. and Ricat, W., (2002): Diabetes; 51: 2348-2354. 29.Kaviarasan, K.;Arjunan, M .M . and Pugalendi, K.V., (2005): Clin. Chem. Acta.; 362:49-56. 30.Baldwin, D.A., Jenny , E.R. and Aisen, P., (1994): J. Biol. Chem.; 259: 13391-13394. 31.Tran, T., Ashraf, M ., Jones, L., Az am, M .H. and Linder, M .C., (2002): J. Nut r.; 123: 351- 356. Table (1): Lipid and li poprotei n parameters in sera of type IIa, type IV HPLic groups and normolipidemic control Parameters Groups TC mg/dl mean±SD P TG mg/dl mean±SD P HDL mg/dl mean±SD P LDL mg/dl mean±SD P Normolip idimic Control n=22 184.3± 11.2 123.7± 9.8 45.8±4.6 117.4±8.7 HPL typ e IIa n=21 365.7± 14.8 P<0.05 179.2± 18.2 P<0.05 41.6±7.3 P<0.05 188.7±21.2 P<0.05 HPL typ e IV n=18 246.8± 12.6 P<0.05 378.9± 11.3 P<0.05 40.7±5.8 P<0.05 129.1±13.2 P<0.05 *P<0.05 *P<0.05 *p <0.05 *p <0.05 * Represent P value between ty p e IIa and IV HPL group s IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 Table(2) :S erum malondial dhyde and free iron in type IIa, type IV HPLic groups and normolipidemic control group Parameters Groups MDA nmol/dl mean ±SD P Serum free iron µg/dl mean ±SD P Normolipidimic Control n=22 16.3± 3.9 98.8 ± 7.2 HPLic type IIa n= 2 1 28.9 ± 4.2 P< 0.05 118.9 ± 9.3 P< 0.05 HPLic type IV n=18 30.3 ± 6.5 P< 0.05 120.2± 10.1 P< 0.05 *P> 0.05 *P> 0.05 * Represent P value between ty p e IIa and IV HPL group s Table (3) : S erum transfe rring , fe rritin and cerul oplasmi n i n type IIa ,type IV HPLic groups and normolipidemic control group Parameters Group s Transferrin µg/dl mean ±SD P Ferritin mg/ml mean± SD P Cerulop las. mg/dl mean ± SD P Normolip idimic Control n=22 268.8 ±13.4 118.3±15.8 18.8±3.7 HPLic Ty p e IIa n=21 270.3±11.7 P>0.05 223.7±19.2 P<0.05 20.1±4.2 P>0.05 HPLic Ty p e IV n=18 267.9±16.3 P>0.05 257.3±22.7 P<0.05 18.7±9.2 p >0.05 *P>0.05 *P<0.05 *p >0.05 * Represent P value between ty p e IIa and IV HPL group s IBN AL- HAITHAM J . FO R PURE & APPL. SC I VO L. 23 (1) 2010 Table(4) HPLic groups and normoli pidemic control group Parameters Groups MDA nmol/dl mean ±SD P Serum free iron µg/dl mean ±SD P Normolipidimic Control n=22 16.3± 3.9 98.8 ± 7.2 HPLic type IIa n= 2 1 28.9 ± 4.2 P< 0.05 118.9 ± 9.3 P< 0.05 HPLic type IV n=18 30.3 ± 6.5 P< 0.05 120.2± 10.1 P< 0.05 *P> 0.05 *P> 0.05 * Represent P value between ty p e IIa and IV HPL group s 2010) 1( 23مجلة ابن الھیثم للعلوم الصرفة والتطبیقیة المجلد وذمسببات االكسدة ومضادات االكسدة البروتینیة ؛االكسدة الفوقیة للدهون من الذكور ارتفاع البروتینات الدهنیة انواع مختلفة من في العالقة وفاء فاضل الطائي جامعة بغداد،هیثملیة التربیة ابن الك،قسم الكیمیاء الخالصة ) 63-48(تتــراوح اعمـارهم بــین شـملت الدراسـة الحالیــة تسـعة وثالثـین مــن الـذكور یعــانون مـن ارتفـاع الــدهون فـي الـدم فضـال عـن، الخارجیـة لمستشـفى بغـداد التعلیمـيالعیادة فيلدهون الدم والمراجعین " خافضا" نهم عالجاسنة ال یتعاطى أي م .مجموعة سیطرة بوصفهم مستویات دهون طبیعیة في أمصالهم مقاربین في العمر يلذكور ذثنین وعشرین من اإ علــى صـــورة الـــدهون " كــرس الجـــزء االول مــن الدراســـة لتصـــنیف الــذكور المصـــابین بارتفــاع الـــدهون فـــي الــدم اعتمـــادا .والبروتینات الدهنیة على موجب معیار محدد والبروتینــات الدهنیــة ،)TG(الكلیســریدات الثالثیـة و ، )Ch(رول الكلــي شــملت الكولسـتصـورة الــدهون و تـم التحــري عــن وافــي أمصـال الـذكور المشـاركین فــي الدراسـة وقـد صــنف) LDL(والبروتینـات الدهنیــة واطئـة الكثافـة،) HDL(عالیـة الكثافـة وثمانیــة ،)IIa(ارتفــاع الكولســتیرول نــوع مـن یعــانون مریضــا وعشــرین اوظهــر ان واحـد Fredericksonعلـى أســس نــوع ).IV(یعانون من ارتفاع في الكلسیریدات الثالثیة نوع اخرینعشر ن عـن طریـق قیـاس المـالون ثنـائي االلدیهایـد عیـین مسـتویات مؤشـر فـوق أكسـدة الـدهو تم في الجـزء الثـاني مـن الدراسـة ت )M DA(، وبالزین في أمصال جمیع الذكور المشاركین في الدراسةسیریلوال،والترانسفرین،والفرتیین ،والحدید الحر. ، الكولسـترول الكلـي والكلســیریدات الثالثیـة والـدهون واطئـة الكثافــةمسـتویات فـي " معنویــا" عـااأظهـرت نتـائج الدراسـة ارتف ) IV(ونــوع ) IIa(فــي مسـتوى البروتینـات الدهنیـة عالیـة الكثافــة فـي أمصـال المجمـوعتین نـوع" معنویـا" بینمـا وجـد انخفاضـا ) IIa(نـوع مجموعتینفي حین لم تظهر فروقات معنویة في مستوى الدهون العالیة الكثافة بین ال،مقارنة مع مجموعة السیطرة ).IV(و IVونــوع IIa مجمـوعتین نــوعالیهایــد والحدیـد الحـر والفـرتین ارتفاعــًا معنویـًا فـي دظهـرت معـدالت المـالون ثنـائي االلأ مقارنـة مـع المجموعـة IVفـي المجموعـة نـوع كذلك وجد أرتفاعـًا معنویـًا فـي مسـتویات فـرتین المصـل، ءع االصحامقارنة م pإن امـل علمـ\ملغــم 19.2±223مقابـل IIa )257.3± 22.7نـوع معنویـة فــي حـین لـم تظهـر فروقـاتفــي ،) 0.05> .IVو IIa بین المجموعتین معدالت المالون ثنلئي االلدیهاید وال الحدید الحر مقارنــة IIaفـي مسـتویات الترانسـفرین والسـیروبالزمین فـي أمصـال مجموعـة النـوع إرتفاعـًا غیـر معنـويً رت النتـائجأظهـ IV مسـتویات الترانسـفرین والسـیروبالزمین فـي أمصـال مجموعـة النـوعوجد إنخفاضًا غیر معنـوي كما، مع مجموعة السیطرة مســتویات الترانســفرین والســیروبالزمین بـــینى لــابالنســبة ات معنویــة بینمــا لــم تظهــر فروقـــ. رنــة مــع مجموعــة الســیطرةامق .IVو IIa المجموعتین الـدم سـواء كـانوا مـن لشد التأكسدي فـي االفـراد الـذین یعـانون مـن إرتفـاع دهـونلترحت هذه الدراسة وجود أضرار نتیجة قا ضـة لالكســدة ر دهون واطئـة الكثافـة التــي تكـون عالــذي قـد یعـزى الــى المسـتویات المرتفعـة للــ IVأو نـوع IIaالمجموعـة نـوع صــورته لالكســدة فـي امولـد والمســتویات المرتفعـة للحدیــد الحـر فــي المصـل الــذي یكـون عــامالأكثـر مــن غیرهـا مــن الـدهون .ةر الح