Influence of turmeric on biochemical disorders induced by exposure to γ- rays or chlorpyrifos pesticide on rats.

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1 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 Influene of turmeri on iohemil disorders indued y exposure to γ- rys or hlorpyrifos pestiide on rts. E. M. Kml El-Dein nd R. M. Erhim * Rdition Biology Deprtment, * Helth Rdition Reserh, Ntionl Centre For Rdition Reserh nd Tehnology (NCRRT), Ciro,Egypt. Reeived: 5/7/2012 Aepted: 20/9/2012 ABSTRACT Toxiity of Chlorpyrifos nd γ-rdition exposure on rts were exmined in the presene or sene of Turmeri (200 mg/ kg/.wt.). Effets hlorpyrifos when dministrted orlly to rts t dose 9 mg/ kg.wt (1/ 4 LD 50 ) for 7 nd 28 dys showed inresed level of mlondildehyde (MDA) onomitnt with depletion in the levels of glutthion (GSH), superoxide dismutse (SOD) nd tlse (CAT).γrdition exposure effet on rts ws exmined in the presene or sene of turmeri. Exposure of rts to γ-rdition (8 Gy) t frtionted dose levels (2 Gy/ week for 4 weeks) exhiited n elevted level of MDA nd deresed level of GSH, SOD nd CAT. Administrtion of Turmeri to nimls whih were previously treted with Chlorpyrifose or γ-rys showed n meliortion response to the ntioxidnt regime. Tretment of rts with Chlorpyrifose for 7nd 28 dys or γ- rdition indued n elevted serum trnsminses level(alt&ast),alkline phosphtse (ALP) nd Aid phosphtse tivitey (ACP), retinine onentrtion, lood ure nd uri id.also tretment of rts with Chlorpyrifose for 7nd 28 dys or γ-rdition indued deline in the testosterone level ssoited with ltertion in the levels of folliulr stimulting hormone (FSH),Iuetinizing hormone (LH) nd proltin (PRL).Results oserved due to Chlorpyrifose pestiide or rdition-exposure hve een meliorted y turmeri dministrtion. It ould e onluded tht turmeri might protet from oxidtive stress. Keywords: Pestiide/ gmm-rdition/ turmeri/ ntioxidnts/ hormones INTRODUCTION Orgnophosphte (OP) insetiides Whih re used in the griulturl nd domesti pest ontrol (1),ount for 50% of the glol insetiidl use (2). Their use is, however, ompnied y widespred toxiity in non-trget orgnisms, inluding mn. Chlorpyrifos (CPF ) is one of the most widely used OP insetiides until 2006 when the United Sttes Environmentl Protetion Ageny restrited some of its domesti uses due to its toxiity. Despite this, CPF remins one of the most widely used OP insetiides. Anemi nd ltertion in other hemtologil prmeters hve een reorded following repeted CPF exposure (3).The mehnism of ute CPF toxiity involves genertion of retive oxygen speies (ROS) nd ltertion of ntioxidnt enzymes tivity in the intoxited rts (4).Turmeri (Curum long L. rhizomes) is onsidered her perennilly ultivted in the Fr Est nd other tropil res. It elongs to the ginger fmil,zingieree.chemilly, it ontins 14% of voltile oil, whih is minly omposed of tlntone,turmerone nd zingierrone.also,this her is omposed of % urumim,28% gluose,12% frutose,1% rinose s well s resins,protein,vitmins nd minerls.the voltile oil omponents nd urumin re onsidered the most tive gents; turmeri hs proved gret del of phrmologil tivity.it 328

2 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 hs een found to exert n effetive ntioxidnt, ntirinogeni, ntinflmmtory nd nti-miroil properties (5).Aordingly,Turmeri is widely used s food dditive mostly ll over the world. Exposure to ionizing rdition uses injuries to the iologil system nd mny defense mehnisms, s enzymes nd ntioxidnt (6).One effet of ionizing rdition is to generte oxygen free rdils,using ell dmge y removing hydrogen tom from ftty ids,resulting in lipid peroxidtion with susequent hnge in memrne fluidity nd permeility. Free rdils re lso ple of using protein oxidtion (7).This investigtion ws designed to test the hypothesis tht Turmeri n provide protetion from CPF nd rdition dmge. A pilot test for deteting the LD 50 : MATERIALS AND METHODS LD 50 ws determined ording to Lithfoeld nd Wiloxon (8) method. LD 50 of Chlorpyrifos ws found to e 36 mg/ kg.wt. of rt. Chlorpyrifos stok formultion (48 % E.C) ws otined from Summitomo Compny (Jpn).It ws determined y diluting 1 ml of stok formultion up to 13.3 ml with orn oil to give the desired LD 50 otined dose. Rdition fility: The soure ws 137 Cesium, Gmm Cell-40 mnuftured y the Atomi Energy of Cnd (Ltd.) provided t NCRRT, Nsr City, Ciro, Egypt. Groups of 14 rts were pled in ventilted plsti ges nd llowed for free movement. Animls were exposed to 8 Gy frtionted dose of irrdition given s 2 Gy weekly for 4 weeks t dose rte of 1 Gy / 2.10 min. Turmeri Tretment : Turmeri ws purhsed from Plnt Protetion Reserh Institute,Agriulture Reserh Center, Egypt. Animl reeived turmeri orlly for 7 onseutive dys efore CPF pestiide or rdition exposure nd tretment ws ontinued during the whole period of irrdition nd CPF proessing (4 weeks).the dministered dose ws 200 mg/kg.wt/dy suspended in 0.5 ml of distilled wter sed on protool desried y Rukkumni et l., (9). Animl groups under investigtions: Adult mle rts (l10± 10g) were otined from the Holding Compny for Biologil Produts nd Vines (VASERA), Ciro, Egypt, housed in speilly designed ges nd llowed to reeive stndrd lned diet nd free wter supply. The nimls were divided into 6 groups (eh of 14 rts): (1): Control group. (2): Rts orlly intuted single dose of 1/4 LD 50 (9 mg/ kg rt) of Chlorpyrifos dily for 4 weeks. (3): Rts sujeted to 8Gy. frtionted doses of γ-rys (2 Gy) one week for 4 weeks. 8 Gy exposure ws strted from the 3 th dy of tretment with CPF. (4): Rts reeived orlly Turmeri for 4 weeks t dily dose of 200 mg/kg.wt., (5): Chlorpyrifos group ws given Chlorpyrifos t dose of 9 mg/kg.wt. fter whih the turmeri hs een orlly dministered. (6): Rts reeived orlly Turmeri nd in the sme time the were exposed to the frtionted gmmirrdition dose (2 Gy weekly). 14 nimls from eh group were srified 24 hours post the end of the experiment. Blood (y rdi punture) ws olleted nd prepred following norml lortory proedures, for the mesurement of the iohemil nd hormonl prmeters. 329

3 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 Biohemil Anlysis: Lipid peroxidtion produt ws mesured using the method of Yoshiok,et l., (10) y the mesurement of MDA s one of the min end produts of LPO. GSH ontent nd SOD tivity were determined following the method reported y Beutler, et l., nd Minmi & Yoshikw (11,12).CAT tivity ws determined ording to the method desried y Johnsson nd Borg (13). AST nd ALT tivities were mesured ording to Reitmn nd Frnkel (14).ALP tivity ws performed ording to method of Kind nd King (15).ACP tivity ws mesured ording to method of Vnh nd Nikkn (16). Ure onentrtion ws mesured ording to the proedure desried y Hllett nd Cook (17) nd retinine onentrtion ording to the method of Fulkner nd King (18).Serum uri id ws determined following the method reported y Brhm nd Trinder (19). Hormonl ssy: Estimtion of testosterone hormone ws rried out using dignosti kit purhsed from DPC ompny s desried y Yen nd Jffe (20), LH hormone ws ssyed with the use of dignosti kit desried y Sntner, et l., (21). Plsm FSH onentrtion ws mesured using doule ntiody rdio-immuno-ssy (RIA) ording to the stndrd method of Snedeor, nd Cohrn (22). PRL hormone ws determined y speifi doule ntiody rdio-immuno-ssy s desried y Djursing (23). The level of the hormones were lulted ording to stndrd urves. Sttistil nlysis: Dt re represented s men± SE. Results otined were sttistilly nlyzed s desried y Sendor (24). Oxidnt nd ntioxidnt levels: RESULTS AND DISCUSSION Dt shown in tle (1) demonstrte tht the tretment of nimls with Chlorpyrifos lone fter 1 week nd 4 weeks reveled signifint inrese of MDA y 111.8%, 108.3% ompred to the ontrol group. Wheres, in the sme group there ws signifint derese in the GSH y 92.4%, 93.6 %, signifint derese ourred in the SOD tivity y 90.3%, 87.9% nd CAT y 82.3%, 91% ompred to the orresponding ontrol vlues. Exposure of rts to γ-rdition exhiited signifint inrese in MDA (120.4%, 117.9%) ompred to the ontrol group. The other iohemil prmeters showed signifint derese (88.9%, 88.2%) for GSH ontent, (88.3%, 90.2%) for SOD tivity nd 75.8%, 77.4% for CAT ompred to the ontrol ones. Tretment of nimls with Turmeri nd in the sme time with Chlorpyrifos pestiide ( t 1 week, 4 weeks), showed n meliortive to effet on the levels of the tested MDA, GSH, SOD nd CAT levels in omprison with those of the Chlorpyrifos group No. 3 rehing (101%,99.3%), (96.4%,98.1%), (95.3%,97.5%), (90.3,%,94 %),respetively. Finlly, the tretment of nimls with Turmeri s well s exposure to γ-rys through the period of experimenttion showed n improvement in the level of MDA, GSH, SOD nd CAT, respetively in omprison with the vlues of the rdition group No. 4 rehing (104%,104%), (93.6%,95.9%), (95.9%, 95.9%), (83%, 90.2 ),respetively. 330

4 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 Tle (1): Influene of turmeri supplementtion to rts on the hzrdous effet of hloropyrifose nd gmm- irrdition on MDA, GSH, SOD nd CAT levels. Group MDA (n mol./ml.) GSH (mg/dl( SOD ( U/ml.) CAT ( U/g ) Time 1 week 4 week 1 week 4 week 1 week 4 week 1 week 4 week ontrol Men 28.8± ± ± ± ± ± ± ±0.53 turmeri Men 28.7± ± ± ± ± ± ± ±0.33 % of hnge 99.6% 100% 100.5% 100.3% 100.6% 100.8% 93.55% 108% hloropyrifos Signifine Men 32.2± ± ± ± ± ± ± ±0.51 % of hnge 111.8% 108.3% 92.4% 93.6% 90.3% 87.9% 82.3% 91% Signifine Rdition Men % of hnge Signifine 34.7± % 34.1± % 47.6± % 47.4± % 39.2± % 40.03± % 18.8± % 18.2± % Turm.+Chlor. Men 29. 1± ± ± ± ± ± ± ±0.51 % of hnge 101% 99.3% 96.4% 98.1% 95.3% 97.5% 90.3% 94% Signifine Turm+Rd. Men 30.01± ± ± ± ± ± ± ±0.39 % of hnge 104% 104.1% 93.6% 95.9% 95.9% 95.9% 83% 90.2% Signifine The vlues re the men of 14 rts± SE. = Signifint when ompred with the ontrol group. = Signifint when ompred with the group treted with pestiide. = Signifint when ompred with the group treted with gmm rys. Chnges in serum ALT, AST, ALP nd ACP: As shown in Tle (2) the tretment of nimls with Chlorpyrifos pestiide lone for 1 week nd 4 weeks reveled signifint inrese in the serum AST, ALT,ALP nd ACP y (171.7 %,171 %), (132.3%,135.8 %),(125.2 % 123.4%) nd(111.4%,113.1%) respetively, in omprison with those of the ontrol ones. Wheres, exposure of rts to -rdition lone, exhiited signifint inrese in AST y( 186.8%,180%), ALT y (137.5%,136.1%),ALP y (129.9%,133.4%) nd ACP y (115.4%,117.4%) respetively, fter 1 week nd 4 weeks ompred to the ontrol ones. Tretment of nimls with Chlorpyrifos pestiide for 1 week, 4 weeks, nd in the sme time reeived Turmeri, exhiited n meliortive effet on the levels of the tested AST, ALT, ALP nd ACP levels in omprison with the Chlorpyrifos group No. 3. Finlly the tretment of nimls with - rdition nd in the sme time injeted with Turmeri, through the experimentl period showed mrked restortion in the level of AST,ALT, ALP nd ACP y (163.9%, 162%), (113.8 %,104.7 %),(117.8,117.8%), (107.8%,111.5%) respetively in omprison with those of the rdition group No

5 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 Tle (2): Influene of turmeri supplementtion to rts on the hzrdous effet of hloropyrifose nd gmm- irrdition on AST, ALT, ALP nd ACP levels. Group AST (U/L.) ALT (U/L.) ALP (U/L.) ACP (U/L.) Time 1 week 4 week 1 week 4 week 1 week 4 week 1 week 4 week ontrol Men 25.8± ± ± ± ± ± ± ±0.80 turmeri Men % of hnge 26.4± % 26.6± % 30.1± % 30.6± % 37.01± % 37.1± % 112.3± % 110.3± % hloropyrifos Rdition Signifine Men % of hnge Signifine Men % of hnge Signifine 44.3± % 48.2± % 43.8± % 46.1± % 39.3± % 41.4± % 40.6± % 40.7± % 45.7± % 47.4± % 44.3± % 47.3± % 122.3± % 126.8± % 123.6± ± % Turm.+Chlor. Turm+Rd. Men % of hnge Signifine Men % of hnge Signifine 37.8± % 42.3± % The vlues re the men of 14 rts± SE. 38.1± % 41.5± % 30.6± % 33.8± % 30.4± % 31.3± % 40.7± % 42.8± % 41.1± % 42.3± % 115.3± % 118.3± % 116.1± % 121.8± % = Signifint when ompred with the ontrol group. = Signifint when ompred with the group treted with pestiide. = Signifint when ompred with the group treted with gmm rys. Chnges in Serum level of Cretinine, Ure nd Uri Aid : As shown in Tle (3), tretment of rts with Chlorpyrifos pestiide for 1 week & 4 weeks reveled signifint elevted levels of renl funtion prmeters y (138.7%,154%), (122.9%,128.6%) nd (135.3%,161.6%) respetively for retinine, ure nd uri id pompred to the ontrol levels. Exposure of nim1s to -rdition doses indued lso highly signifint inrese in renl funtion prmeters y 161.2%,166%for retinine, 131%,135.3% for ure nd 150%,181.6% for uri id ompred to the ontrol levels.tretment of rts with Chlorpyrifos pestiide for 1 week &4 weeks, nd in the sme time dministered turmeri, renl funtion prmeters eome etter in omprison with the levls the Chlorpyrifos group No 3. Tretment of nimls with -rdition through the experimenttion period nd in the sme time ingested with Turmeri,showed n improvement tion on the renl funtion prmeters in omprison with the rdition group No. 4, rehing 108.1%, 128% for retinine, 109%,115% for ure nd 102.9%,108.3% for uri id respetively. Hormonl levels ssy: Results presented in tle (4), disply tht the tretment of rts with Chlorpyrifos pestiide for 1 week &4 weeks indued signifint derese in the testosterone level (75.5 %, 67%), ompred with the orresponding ontrol level. Also, the tretment used signifint inrese in the FSH level y 171.9%, 172.5%, LH level y 110.6%, 122.4% nd PRL hormone level y106.8%, 117.6%, ompred with ontrol group. Exposure of nimls to -rdition showed highly signifint deline in the ontent of testosterone (69.6%, 58.6%) ompred to the ontrol level. Menwhile, the levels of FSH, LH nd PRL in the sme group reveled signifint ugmenttion in their levels (183.1%, 332

6 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) %), (139.5%, 142.5%), (106.4%, 114.9%) respetively ompred to the ontrol vlues. Tretment of nimls with Chlorpyrifos. Tle (3): Influene of turmeri supplementtion to rts on the hzrdous effets of hloropyrifos nd gmm- irrdition Cretinine, Ure nd Uri id levels. Group Cretinin (mg/dl) Ure (mg/dl) Uri id (mg/dl) Time 1week 4 weeks 1week 4 weeks 1week 4 weeks Control Men 0.49± ± ± ± ± ±0.35 Turmeri Chloropyrifos Rdition Men % of hnge Signifine Men % of hnge Signifine Men % of hnge Signifine 0.47± % 0.68± % 0.79±0.03 % ± % 0.77± % 0.83±0.06 % ± % 36.01± % 38.5±0.46 % ± % 36.8± % 38.7± % 5.9± % 9.2± % 10.2± % 5.8± % 9.7± % 10.9± % Turme+Chlorp Men 0.58±0.37 % of hnge 118.3% Signifine Turme.+Rd Men 0.53±0.22 % of hnge 108.1% Signifine The vlues re the men of 14 rts± SE. 0.51± % 0.64± % 31.3± % 32.9± % 32.3± % 32.9± % 8.4± % 7.01± % 7.8± % 6.5± % = Signifint when ompred with the ontrol group. = Signifint when ompred with the Chloropyrifose group. = Signifint when ompred with the Rdition group. Pestiide nd in the sme time delivered Turmeri, reveled miliortion in the levels of the tested hormones (testosterone, FSH,LH nd PRL ) y 91.7%, 96.2 %, 137.6%, 124.1%, 107.1%, 111.7% nd 101%, 101.8% respetively in omprison with the Chlorpyrifos group No.3 levels. The exposure of nimls to -rdition nd the sme time treted with turmeri improved the levels of the tested prmeters ompred with those of the rdition group No.4 333

7 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 Tle (4): Influene of turmeri supplementtion to rts on the hzrdous effets of hloropyrifose nd gmm-irrdition on Testosterone, FSH, LH, nd PRL. Groups Testosterone (ng/ ml) FSH (ng/ml LH (miu/ml PRL (miu) Time 1week 4 week 1week 4week 1week 4week 1week 4week Control Men 2.54± ± ± ± ± ± ± ±0.05 Turmeri Men % of hnge 2.57± % 2.51± % 3.27± % 3.35± % 2.77± % 2.74± % 4.70± % 4.48± % Chloropyrifos Signifine Men % of hnge Signifine 1.92± % 1.75± % 5.52± % A 5.71± % 3.11± % 3.22± % 4.98± % 5.20± % Rdition Turme+Chlorp Turme.+Rd Men % of hnge Signifine Men % of hnge Signifine Men % of hnge Signifine 1.77± % 2.33± % 2.17± % 1.53± % 2.61± % 2.49± % 5.88± % A 4.42± % A 4.91± % 5.91± % 4.11± % 4.55± % 3.92± % 3.01± % 3.31± % 3.75± % 2.94± % 3.46± % 4.96± % 4.71± % 4.46± % 5.8± % 4.50± % 4.63± % The vlues re the men of 14 rts± SE. = Signifint when ompred with the ontrol group. = Signifint when ompred with the Chloropyrifose group. = Signifint when ompred with the Rdition group. Oxidtive stress is known to e disprity etween the rtes of free rdil prodution nd rte of elimintion (25). Exposure to ionising rdition eventully results in injuries to the iologil systems depending on the dose, durtion nd type of rdition exposure nd rdio-sensitivity of vrious tissues. It hs een onformed tht 6 Gy γ-rys lter hemil spets in rts (26).Bshir et l., (27) reported tht propgtion of LPO in iologil memrnes, ompnied y the dysfuntion of the ntioxidnt system nd depletion of GSH, were ttriuted to pestiide toxiity tht my use exessive prodution of free rdils. In the present study, dministrtion of Chlorpyrifos pestiide to mle rts dy/ for 1 week, nd 4 weeks ould enhne the oxidtive stress tht ws ompnied y ugmenttion of LPO nd depletion of GSH ontent, SOD nd CAT tivity. The ntioxidnt defensive mehnism in rts is hrterized y hroni inflmmtory syndrome ssoited with severe oxidtive dmge of lipid moleules nd depleted ntioxidnt pity (28). Consequently, drmti fll hs ourred in GSH leding to memrne LPO in Chlorpyrifos pestiide nd γ-irrdited groups. The ove mentioned results re in hrmony with present findings in whih Chlorpyrifos pestiide nd γ-rys ould use elevtion in MDA level nd redution in GSH ontent, SOD nd ACT tivity. The vitl importne of Turmeri for helth nd s reduing gent of oxidtive stress is now fully reognized nd it hs een tested for their rdioprotetive effets on different nimls (29). In the present study, Turmeri intke modulted the dngers of Chlorpyrifos pestiide nd γ- rys nd resulted in superior therpeuti effet nd give rise to non-signifint differenes in MDA, GSH, SOD nd CAT levels in omprison with ontrol groups. In the present study, the exposure of 334

8 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 rts to the pplied dose level of Chlorpyrifos pestiide for 1 week, 4 weeks indued signifint elevtion in serum trnsminses level. This inrese ould e ttriuted to heptoellulr impirment whih susequently used the relese of greter levels of intrellulr enzymes into the lood s result of mssive dmge of liver nd other orgns. The elevtion in the liver enzymes tivity my e due to insuffiieny of ATP whih is neessry s n energy soure for uilding protein nd mino ids.chlorpyrifose is well sored y ingestion, inhltion nd skin ontt nd metolized in liver y mirosoml xenoioti metolizing enzymes..hene oth hlorpyrifose nd hlorpyrifose oxon (orgnophosphours ompounds) re toxi ompounds nd hve hrmful effet on liver (30).The toxiity of orgnophosphorus insetiides vries depending on the route of dministrtion,vehile.speies nd sex (31). Exposure of dult rts to gmm-rdition dose exhiited signifint inrese in the level of serum ALT,AST,ALP nd ACP whih ould e onsidered n indition to the toxiity indued y rdition exposure.these results re in greement with those previously reported Kpln (32). The inrese in serum level of these enzymes my e due to ltertion in the dynmi permeility of memrnes y ionizing rdition, llowing lekge of iologil tive mteril out of the injured ell,whih my e ssoited with ell deth or injuries.also, ALP is onsidered s n enzyme of the heptoytes plsm memrne,thus n inrese in serum ALP tivity hs een relted to dmge of liver ell memrnes (33). Exposure of rts to ionizing rdition eventully results in injuries to the iologil systems depending on the dose, durtion nd type of rdition exposure, the rdiosensitivity of different tissue esides severl other importnt ftors (34). In the present study, the tretment of rts with Chlorpyrifos pestiide doses for 1 week nd 4 weeks nd exposed to - rdition doses displyed signifint elevtion in the serum renl funtion prmeters (retinine, ure nd uri id). These results re in ordne with the results of Roins, et l., (35). Who reported n inrese in the lood retinine level in the irrdited rts.they reported lso tht irrdition of rts t dose level from 6-13 Gy indued extensive retention in dily exreted urine whih result in retinuri tht led to inrese in its level in the lood. They ttriuted this tion to the intertion of retinine with their sites of iosynthesis. The exposureof nimls to ionizing rdition indue protein rekdown mnifested y n inrese in the protein endproduts. Ure eing the mjor end-produt of protein tolism.the degrdtion of protein y ionizing rdition exposure is ompnied y n inrese in the serum ure in nimls exposed to - rdition nd therefore inrese in the free mmoni in different tissues (36). Also, sustining tht result of the inresed rte of protein tolism in nimls exposed to - rdition, tht led to inresed ure level. In the present investigtion inresed serum uri id ould e n indition of renl disese nd elevted serum uri id my lso reflet metoli defet in purine metolism tht used inresed prodution of uri id. The inrese in lood ure level ould e t ttriuted, in prt, to n impirment of kidney funtion. The present dt re in hrmony with erlier reports doumenting elevted serum ure fter tretment with different pestiides. Aute doses of 2, 4- dihlorophenoxueti id t levels of 100, 300 nd 600 mg/kg ody weight inresed serum ure in rts (37) nd dily orl exposure of the syntheti pyrethroid ypermethrin produed signifint inrese in serum ure nd retinine in rts (38). The pestiides used signifint inrese in oth retinine nd ure levels. These results onord those of Aly et l., (39) who stted tht orl dministrtion of the insetiide deltmethrin t 13 mg/kg or 26 mg/kg to mle rts for 28 onseutive dys used signifint inrese in retinine nd ure levels. 335

9 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 In the present study, the exposure of nimls to Chlorpyrifos pestiide s well s -rdition exhiited mrked derese in the testosterone level nd signifint inrese in the level of FSH nd LH due to the effet of the used pollutnt (40). The seretion of testosterone is under the ontrol of LH nd the mehnism y whih LH stimultes the leyding ells involves inrese formtion of yli AMP. Testosterone is lso formed in the drenl ortex. Ninety-seven perent of the testosterone plsm is ound to protein: 40%is ound to B-gloulin nd lled gondl steroid inding nd 40% to lumin nd 17% is ound to other proteins (41). The derese in the level of testosterone ompnied with n trophy in sex gonds ws reveled y the destrution tht ourred in the germinl ells of testis fter exposure to pestiides or gmm rys.similrly, signifint derese in the testosterone level fter tretment of rts with quinlphos or melthion.this deline oud e due to the inhiition of formtion of 5-lph-DHT whih led to derese in the level of ndrostnedione. Reently, some uthors ttriuted this derese to the toxi effet of pestiides diretly nd/or indiretly vi hypothlmi pituitry testis xis nd the derese in the testosterone onentrtion whih ws dependent on oth dose nd time of exposure (42). FSH my lso ugment testosterone seretion possily y induing mturtion of the leyding ells. Testosterone lso regultes the sensitivity of the pituitry to the hypothlmi-relesing ftor luteinizing hormone-relesing hormone (LHRH). Although the pituitry n onvert testosterone to dihydro testosterone nd/or to estrogens, testosterone itself is the primry regultion of gondotrophin seretion (43). Testosterone redues plsm LH ut expet in lrge doses, it hs no effet on the plsm FSH. Thus, it ppers tht testosterone feeds k to inhiit LH seretion, wheres FSH seretion is independently ontrolled y inhiin protein sereted y sertoli ells nd ts on the pituitry glnd diretly (44). In response to LH, some of the testosterone sereted from the leyding ells thes through the seminiferous epithelium lyer nd provides the high lol onentrtion of ndrogen systemilly (41). The present oservtions mth those found y (44). Who reported tht hzrds indution y irrdition nd of hemotherpy on the tivity of sertoli ells led to the destrution of germinl epithelium. They further stted tht gondl dmge pper fter frtionted irrdition doses. The implition of gondl dysfuntion indued y hemotherpy or irrdition go eyond the dignosis of menorrhe nd ltered gondotrophin prmeters. The nturlly ourring polyphenoli ntioxidnt hve reeived inresed ttention in the mintenne of helth nd in disese prevention (45). Reently, there hs een n inresing interest in the protetive funtion of dietry ntioxidnts, whih re ndidtes for the tretment of theroslerosis, ner hemoprevention nd extending lifespn (46).Severl ntioxidnts, suh s vitmin E,vitmin C, B-rotene, uri id nd flvonoids, hve een found to to ply importnt rols in the non-enzymti protetion ginst oxidtive stress. Turmeri hs een reported to posses rod spetrum of hemopreventive tivity in prelinil models nd ppers to e sfe in niml nd humn studies (47). In the present study, experimentl nimls reeiving 200 mg/hg ody wt. Turmeri, for 4 weeks indued meliortive tion on the redox system (Tles 1, 2, 3, 4). Turmeri undergoes extensive metoli onjugtion nd redution in the gstrointestinl trt in humns nd rts. Turmeri exerted through free rdils svenging property nd eletron hydrogen dontion mehnism (48).Moreover, the ntioxidnt mehnism of turmeri is ttriuted to its unique onjugted struture, whih inludes two methoxylted phenols nd n enol form of B-diketone; the struture shows typil rdil-trpping ility s hin- reking ntioxidnt (49). In the present study, dministrtion of turmeri to irrdited rts hs signifintly meliorted the hnges indued y irrdition nd pestiide exposure supporting the hypothesis tht plnt produts re effetive ntioxidtive gents, y svenging or neutrlizing free rdils interting with oxidtive sde nd preventing its outome quenhing singlet oxygen mking it less ville for oxidtive retion (50) ; inhiiting oxidtive enzymes lik ytohrome P450 nd y helting metl ions like Fe,inhiits peroxidtion of memrne lipids nd mintins ell memrne integrity nd their funtion (51). Furthermore, (52) found tht, onversion of XD to XO is redued y turmeri to the sl level in vitro study. It is suggested tht, the mjor inhiitory mehnism of turmeri on inreses in XO enzyme tivities is through diret intivtion t the protein 336

10 Ar Journl Of Nuler Siene And Applitions, 46(1), ( ) 2013 level.therefore, turmeri my stilize the ell memrne nd signifintly redue the extent of lipid peroxidtion in the lood nd liver indued y oxidtive stress-relesed under influenes of gmm rdition nd Chlorpyrifose pestiide. CONCLUSION The development of proedures to meliorte undesirle ROS prodution my e one of the entrl issues in reserh on ging nd oxidtive stress-relted diseses in the ner future. Dietry ntioxidnt re widely used to meliorte exessive oxidtive stress; despite sientifi proof of their effiy is sre ( 53 ).However, the ntioxidnt nd ytoprtetive tivites indued y turmeri offers gret dvntge for therpeuti purposes, nd ould eome prt of dily diet s herl supplement. REFERENCE (1) D. Donldson, T. Kiely, A. Grue. Environmentl Protetion Ageny, Wshington, DC, USA (2002). (2) J. E. Csid, G. B. Quistd. Chemil Reserh in Toxiology; 17(8),: (2004). (3) A. Goel, V. Dni, D. Dhwn. BioMetls.; 19(5): (2006). (4) S.S. Annd, J.V. Brukner, W.T. Hines, S. Murlidhr, J.W. Fisher nd S.Pdill. Toxiol. Appl. Phrmol; 212(2): (2006) (5) N.K. Leel, A. Tv, P. M. Shyi, S.P. john nd B. Chempkm; At.Phrm; 52: (2002). (6) M. Tjuddin, S. Kumr, M. Triq, S. Tygi nd R. Gupt; Ady. Myordiol., 2,233 (1980). (7) E. Vlk nd G. Hornstr; A review.int.j. 22 (2):200. (2000). (8) D. Lithfoeld nd F. Wiloxon; J. phrm. Exper. Therpy, 95: (1949). (9) R. Rukkumni, A. Vrm, K. Rjsekrn, nd V. Menon;J. Phrm. Phrmeul.Si.,7(2): 274 (2004). (10) T. Yoshiok, T. Kwd, T. Shimd nd M. Mori; Am. J. Ostetr. Gyneol, 135: (1979). (11) E. Beutler, O. Durn nd M. B. Kelly ; J. Lo. Clin. Med., 61: (1963). (12) M. Minmi nd H. Yoshikw; Chemi At., 92: (1979). (13) L.H. Johnsson nd H. L. Borg ; Ant.Biohem.,174,331(1988). (14) S. Reitmn nd S. Frnkel; Am. j. Clin.Pthol., 28(1):56 (1957). (15) D.P. Kind nd E.G. King ;Prtil linil iohemistry In: (H.Vrly: A.H.Gownlok nd M. Bell,eds) 5 dys.edition,willim Heinmnn Medil Ind,London,892(1952). (16) T. P. Vnh nd T. V. Nikknen; At Endorino.72: (1973). (17) C.T. Hllett nd J. G. Cook; Clin.Chim.At., 35(1): 33(1977). (18) W. Fulkner nd J King; In: Fundmentls of Clinil Chemistry, 2 dn ed.(n.w.tietzm Ed.) Sunders, Phildelphi, P.994 (1976). (19) D. Brhm nd P. Trinder; Anlyst.97, 142 (1972). (20) S.S. Yen. nd R.B. Jffe ; Edd, Reprodutive Endorinology. (W.B. Sunders).(1978). (21) S. S. Sntner, R. O. Kulin nd L.T. Demers; Clin. Chem., 27(11): (1981). (22) G.W. Snedeor, nd W.G. Cohrn; Sttistil Methods ' 7 ' ed. Two Stte University press, Ames Low, U.S.A (1982). (23) H.Djursing ; At Endorinol., 97,1-6(1981). (24) A. Sendor; Sttistil methods-the Iow Stte University Press, USA.(1969). (25) A. Zhrn, D. Hssn nd M. Medht; Egypt. J. Rd. Si. Appli., 17(1): (2004). (26) S. S.Twfik, M.I. Ady, A.M. Zhrn nd A.K.M. Aouelll ; Egypt. J. Rd. Si. Appli., 19(1): 1-22(2006). (27) F. Bshir, T. O. Siddiqi nd M. Iql; Environ. Pollut. 147(1): (2007). (28) M. Ady, M. Ahmed nd S. Zkri; Egypt. J.Rd.Si. Appli., 16 (1): (2003). (29) H. Li, Y. Cheng, H. Wng, H. Sun, Y. Liu, K. Liu nd S. Peng;. App. Rd. Isotop., 58(3): (2003). 337

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