Cd、Pb对蟾蜍肝脏超氧化物歧化酶活性及其同工酶的影响

以腹腔注射法分别对蟾蜍(Bufobufogargarizans)给Cd和Pb (按镉计0 . 2、0 . 4、0 . 8、1 .6mg/kg体重;按铅计2、4、8、16mg/kg体重) ,连续染毒7d后,观察不同浓度Cd、Pb染毒条件下的蟾蜍肝超氧化物歧化酶(SOD)活性及其同工酶的变化。结果表明:在0 . 2mg/kg、0 4mg/kgCd和4mg/kg、8mg/kg和16mg/kgPb染毒,下蟾蜍肝SOD活性被显著诱导(P <0 . 0 5 ) ;前者酶带2 (Rf=0 . 4 3)活性增强,且均比对照增加1条新酶带(Rf=0 . 38) ;后者只表现为酶带1(Rf=0 . 5 1)和酶带2 (Rf=0 . 4 3)活性的增强,无新酶带的出现。     

镉、铅对蟾蜍精巢毒作用的酶学研究

为研究镉、铅对精巢的生化毒作用机理 ,应用氯化镉、硝酸铅溶液对成年雄性蟾蜍进行腹腔染毒 (按镉计 0 .1、0 .2、0 .4、0 .8mg/ kg体重 ;按铅计 1、2、4、8mg/ kg体重 ) ,连续染毒 7d后活体解剖 ,测定分析精巢中各种酶的活性。结果显示 ,在镉染毒下 ,精巢乳酸脱氢酶 (L DH)和酸性磷酸酶 (ACP)的活性随镉染毒剂量的增加而降低 ,而碱性磷酸酶 (AL P)未发现明显变化 ;在铅染毒下 ,乳酸脱氢酶 (L DH)和碱性磷酸酶 (AL P)的活性随铅染毒剂量的增加而降低 ,而酸性磷酸酶 (ACP)未发现明显变化 ;乳酸脱氢酶 (L DH)同工酶在镉、铅染毒下则主要表现为酶带 L DH1 、L DH2 的抑制或缺失和 L DH5活性的增强。因此 ,镉、铅对蟾蜍的雄性生殖毒性机理可能与酶的活性存在着一定的关系 ,L DH可以考虑作为反映镉、铅中毒对精巢功能影响程度的一种有价值的生化指标     

镉长期暴露对黑斑蛙的氧化胁迫和抗氧化能力的影响

在实验条件下,将黑斑蛙暴露于12．5mg／L和25．0mg／L浓度的镉溶液中30d,分别测定了黑斑蛙在暴露10、20和30d时肝、肾组织中镉（Cd）含量、过氧化产物丙二醛（MDA）的含量、还原型谷胱甘肽（GSH）含量和超氧化物歧化酶（SOD）活性,以探讨镉对机体的脂质过氧化作用及机体的抗氧化损伤机制。实验结果表明,不同剂量组黑斑蛙肝、肾镉含量、MDA含量均随着镉暴露时间的延长而升高,且肝MDA含量与镉在肝中的蓄积量呈显著正相关（R^2=0．8643,n=9）。肝脏GSH含量随镉暴露时间的延长而被显著诱导,且与MDA含量呈显著正相关（R^2=0．5933,n=9）;肾GSH含量则随暴露时间的延长而显著下降,与MDA含量呈显著负相关（R^2=0．8609,n=9）。不同剂量组肝SOD活性随镉暴露时间的延长而升高,肾SOD活性在高剂量组随镉暴露时间的延长表现为先升高后回落下降的趋势。可见,在镉的长期暴露下,细胞膜过氧化增强是镉伤害机体的主要原因,而GSH含量、SOD活性的升高则可能是机体抗过氧化的机理之一。     

铅对蟾蜍肝、肾过氧化物酶和酯酶同工酶的影响

以腹腔注射法对蟾蜍 (Bufobufogargarizans)给铅 ,处理 7d后 ,使用聚丙烯凝胶垂直平板电泳法 ,研究了不同浓度 (按铅计 1、2、4、8mg·kg-1 体重 )的铅对蟾蜍肝脏、肾脏过氧化物酶和酯酶同工酶的影响。结果表明 ,不同浓度的铅均可使肝、肾组织过氧化物酶同工酶带强弱发生明显变化 ;对肝、肾酯酶同工酶的影响表现出一定的组织差异性 ,且在一定范围内主要表现为应激性 ,即低剂量的铅可诱导酶活性的提高。     

镉诱导的菊芋幼苗膜脂过氧化和抗氧化酶活性及过氧化物酶同工酶的改变

用含有不同浓度(0~400μmol/L)Cd(NO3)2的Hoagland营养液处理砂培的菊芋。处理50d后,测定植物体内镉积累量以及过氧化物酶(POD)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性,并对POD同工酶进行电泳分析。发现在Cd50~100μmol/L浓度内,随着镉浓度的升高,菊芋根和叶中镉的积累量显著增加,而随后积累量的增加有所减少。根和叶中MDA含量显著上升,说明镉引起了膜脂过氧化。0~100μmol/LCd处理,根和叶中POD活性随Cd浓度增加而增强,而在200~400μmol/LCd处理下有所减弱。根和叶SOD活性在50~200μmol/LCd处理下随Cd浓度增加而增强,而在400μmol/LCd处理下SOD活性明显受到抑制。根和叶CAT活性随Cd浓度升高而增强。电泳结果显示,POD同工酶变化明显,镉诱导出一条新酶带LP10。菊芋POD同工酶可以作为镉污染的土壤的生物指示剂。     

酮康唑对小鼠肝脏和睾丸生理功能的影响*

目的: 观察不同剂量的酮康唑(KCZ)对昆明小鼠的肝脏和睾丸生理功能的影响。方法: 将 40 只雄性昆明小鼠随机分为 4 组(n=10):正常组、酮康唑低剂量组(30 mg/kg)、酮康唑中剂量组(50 mg/kg)、酮康唑高剂量组(70 mg/kg)。药物组小鼠按0.1 ml/10 g给药体积每日单次皮下注射酮康唑,酮康唑低、中、高剂量组药物浓度各为3 mg/ml、5 mg/ml、7 mg/ml,正常组注射等量生理盐水,连续 3 周。测定血清谷草转氨酶(AST)、谷丙转氨酶(ALT),以及睾丸组织 γ-谷氨酰胺转肽酶(γ-GT)、乳酸脱氢酶(LDH)和酸性磷酸酶(ACP)活性;HE 染色观察肝脏、睾丸病理组织改变。结果: 与正常组比较,酮康唑组AST、ALT活性显著升高(P＜0.01);γ-GT、ACP、LDH活性显著下降(P＜0.01),且以上指标的改变均随剂量增加而损伤加重。HE 染色显示小鼠肝细胞变性,排列松散,胞质色浅;睾丸曲细精管管腔增大,各级生精细胞、精子数量减少。结论: 酮康唑能导致小鼠肝脏、睾丸组织生理功能损伤与病理组织学改变,升高肝转氨酶水平,降低睾丸特异性酶活性,且损伤程度随剂量的升高而增大。     

大豆黄酮对衰老小鼠脑组织SOD、LDH同工酶的影响

利用SOD和LDH同工酶电泳分析,研究大豆黄酮对衰老小鼠的抗氧化作用。结果显示大豆黄酮没有改变SOD和LDH同工酶谱的特征,但对因衰老引起的小鼠脑组织LDH和SOD同工酶活性、各组分的相对活性和比活力的变化有不同程度的改善作用,即LDH同工酶中LDH-2、LDH-3的活性明显下降,LDH-1的活性下降最为明显,而LDH-4的活性有所下降,但不显著,LDH-5的活性几乎没有变化,SOD同工酶的SOD-1和SOD-2的活性有不同程度的升高。这表明大豆黄酮是通过抑制LDH同工酶H亚基的合成来降低LDH的活性,而对M亚基的合成没有影响,并且能够促进SOD同工酶SOD-1和SOD-2的合成,不影响其遗传稳定性。     

阿维菌素对黑斑侧褶蛙毒理效应的研究

本文选用生物农药阿维菌素作为染毒试剂,以农田中常见黑斑侧褶蛙Pelophylax nigromaculatus为研究对象,分别从急性毒性、亚急性毒性、遗传毒性和生理毒性四个方面的实验综合探讨了阿维菌素对黑斑侧褶蛙的生态毒理学效应。急性毒性实验结果表明,阿维菌素对黑斑侧褶蛙24h、48h、72h、96h的LC50分别为:0.3227mg/L、0.0966mg/L、0.0623mg/L、0.0432mg/L,其对黑斑侧褶蛙的安全浓度(SC)为0.004316mg/L。亚急性毒性实验结果表明,暴露期间,随着浓度的升高,毒害作用越大,其对黑斑侧褶蛙肝脏组织损害也越大,而经恢复期后,各实验组肝脏组织受损程度较暴露期都有降低。红细胞核异常及微核诱导实验结果表明,微核和核异常现象与阿维菌素浓度的相关性有一定的范围;随着时间的延长,红细胞核异常率及微核率先上升后下降。肝脏LDH同工酶聚丙烯酰胺凝胶电泳实验结果表明,在一定时间条件下,随浓度的升高,LDH1和LDH2酶带活性呈现降低趋势,LDH4酶带活性无明显变化,LDH5酶带活性先升高后再降低,在同一浓度条件下,随着时间的延长,肝脏LDH同工酶活性均呈升高的趋势。实验结果表明阿维菌素对黑斑侧褶蛙能够造成不同程度的生理、病理及遗传性损伤。     

中国林蛙早期胚胎发育过程同工酶的研究

本文采用聚丙烯酰胺凝胶电泳方法,对中国林蛙（Rana chensinensis)早期胚胎发育过程中（受精后0－512h)乳酸脱氢酶（LDH）同工酶和酯酶（EST）同工酶进行了研究,结果表明：1．LDH同工酶在受精卵及早期胚胎发育过程中一直存在,并且在胚胎发育的不同时期差异显著,LDH1同工酶在胚胎发育的各个阶段都占绝对优势,而DH5活性从尾芽期开始增强,LDH2,LDH3,LDH4 3种同工酶的活性较;低同时也发现LDH1,LDH3,LDH4同工酶各亚带也发育阶段的特异性,2．EST同工酶在开口期才开始出现。     

箭舌豌豆根系抗坏血酸及相关酶对镉胁迫的响应

以箭舌豌豆(Vicia sativa L.)品种L3(耐镉)和ZM(镉敏感)为材料,研究了不同程度镉胁迫下箭舌豌豆幼苗根系抗坏血酸(AsA)含量、脱氢抗坏血酸还原酶(DHAR)同工酶活性、抗坏血酸过氧化物酶(APX)同工酶活性以及APX基因表达的变化。结果显示:(1)2个箭舌豌豆品种根系AsA和脱氢抗坏血酸(DHA)含量在镉胁迫下显著升高;AsA/DHA比值在镉耐性品种L3中显著升高,在敏感品种ZM中显著下降;相同镉处理浓度下,L3根系AsA含量和AsA/DHA比值显著大于ZM。(2)2个品种根系DHAR的活性电泳共显示4条同工酶条带,它们的活性均随镉处理浓度的升高而升高;其中DHAR1只在L3显示,DHAR4只在ZM显示;相同镉处理浓度下,品种L3的DHAR的总活性大于品种ZM。(3)2个品种根系APX的活性电泳共显示11条同工酶条带,其中的APX1、2、4仅在敏感品种ZM中受镉胁迫诱导,APX 8在耐性品种L3中受到比敏感品种ZM更显著的诱导;克隆得到1个箭舌豌豆APX基因,荧光定量RT-PCR结果显示该基因的转录在L3和ZM根系均受镉处理诱导。研究表明,镉胁迫下2个箭舌豌豆品种根系AsA含量,AsA代谢相关酶DHAR和APX的活性以及APX的转录水平均显著升高;镉耐性品种L3较敏感品种ZM能更有效地促进AsA循环,维持更高的AsA水平,从而更有效地缓解镉胁迫诱导产生的氧化胁迫,这可能是L3较ZM具有更高镉耐性的重要机制之一。     

柱状田头菇菌丝对镉胁迫的抗氧化响应

研究了不同浓度Cd处理对柱状田头菇菌丝抗氧化酶及谷胱甘肽含量的影响.结果表明,在低浓度范围内随着Cd处理浓度的增加,菌丝抗氧化酶的活力上升,过氧化氢酶(CAT)与超氧化物歧化酶(SOD)的活性分别在Cd浓度为0.1和0.4mmol·L-1时达最大值;过氧化物酶(POD)、谷胱甘肽还原酶(GR)和脂氧合酶(LOX)的活性在Cd浓度为0.2mmol·L-1时达到峰值.而在高Cd浓度处理时,柱状田头菇菌丝抗氧化酶系(POD、CAT、SOD等)显著受到抑制.0.4~1.6mmol·L-1Cd处理可显著提高菌丝体内还原型谷胱甘肽(GSH)水平,却不影响氧化型谷胱甘肽(GSSG)含量.在整个试验过程中,均未检测到抗坏血酸及抗坏血酸过氧化物酶(APX)的活性.用聚丙烯酰胺凝胶电泳分析Cd胁迫下柱状田头菇菌丝抗氧化酶的同工酶谱发现,0.1~0.8mmol·L-1Cd处理可诱导过氧化物酶(POD)、酯酶(EST)和脂氧合酶(LOX)新同工酶的表达,提高组成型过氧化氢酶(CAT)、超氧化物歧化酶(SOD)同工酶的表达强度;1.6mmol·L-1Cd处理显著抑制POD、CAT、SOD等的表达.     

Effect of chronic cadmium exposure on antioxidant defense system in some tissues of rats: protective effect of selenium

The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl(2) for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na(2)SeO(3) for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage.     

The Effect of Selenium on the Cd-Induced Apoptosis via NO-Mediated Mitochondrial Apoptosis Pathway in Chicken Liver

Cd-induced apoptosis and the protective effects of Se against Cd-induced injury have been reported in previous studies. However, little is known regarding the effects of Cd-induced apoptosis in hepatic cells and the antagonistic effects of Se on Cd in poultry. In the present study, 128 healthy 31-week-old laying hens were randomly divided into four groups, which were fed basic diets, with the addition of Se (Na₂SeO₃, 2 mg/kg), Cd (CdCl₂, 150 mg/kg), or Se + Cd (150 mg/kg of CdCl₂ and 2 mg/kg of Na₂SeO₃) for 90 days. Ultrastructural changes, nitric oxide (NO) concentrations, inducible nitric oxide synthase (iNOS) activities, results of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay of apoptosis, and the expression of iNOS and apoptosis-related genes in livers were determined. It was observed that Cd treatment significantly increased the concentrations of NO and iNOS activity in chicken livers. The production of excessive NO initiated the mitochondrial apoptotic pathway. Exposure to Cd increased the mRNA and the protein expression levels of iNOS, caspase-3, Bax, p53, and Cyt-c. Furthermore, the ratio of Bax/Bcl-2 increased, while the expression of Bcl-2 decreased. Treatment with Se significantly alleviated Cd-induced apoptosis in chicken livers, as evidenced by a reduction in the production of NO, iNOS activity, the number of apoptotic cells, and mRNA and protein expression levels of iNOS, caspase-3, Bax, and Cyt-c. It indicated that Cd induced NO-mediated apoptosis through the mitochondrial apoptotic pathway and Se exerted antagonizing effects. The present study provides new insights as to how Se affects Cd-induced toxicity in the chicken liver.     

中华姬鼠与大林姬鼠的同工酶差异

中华姬鼠（Ａｐｏｄｅｍｕｓｄｒａｃｏ）和大林姬鼠（Ａｐｏｄｅｍｕｓｐｅｎｉｎｓｕｌａｅ）是形态学上十分相似的两种鼠类。为了对两种姬鼠的分类提供生物化学方面的依据,采用聚丙烯酰胺凝胶等电聚焦电泳方法比较和分析了两种姬鼠的ＬＤＨ同工酶、ＥＳＴ同工酶和ＳＯＤ同工酶的差异。结果表明,两种姬鼠的ＬＤＨ同工酶酶谱基本相似,而ＥＳＴ同工酶和ＳＯＤ同工酶酶谱则存在明显的种间差异。根据ＥＳＴ同工酶Ａ２带的有无和ＳＯＤ同工酶主带等电点的差别,能将两种姬鼠很容易区分开来。     

Cadmium toxicity related to cysteine metabolism and glutathione levels in frog Rana ridibunda tissues

The level of glutathione and sulfane sulfur and sulfurtransferases activity in adult frogs Rana ridibunda were investigated after the exposure to 40 mg or 80 mg CdCl(2) L(-1) for 96 h or 240 h. Cd accumulation in the liver, kidneys and testes was confirmed, and the highest Cd level was found in the testes. In the liver, the exposure to Cd resulted in an increase of GSH level and the activity of rhodanese, while the activity of 3-mercaptopyruvate sulfurtransferase and cystathionase decreased. The kidneys and brain showed the elevated level of GSH and the activity of all investigated sulfurtransferases, as well as sulfane sulfur especially in brain. In such tissues as the testes, muscles and heart, the level of GSH and the activity of 3-mercaptopyruvate sulfurtransferase were significantly diminished. The increased level of sulfane sulfur was determined in the testes and muscles and the increased activity of rhodanese in the testes and the heart. These findings suggest the possible role of sulfane sulfur and/or sulfurtransferases in the antioxidation processes, which can be generated in cells by cadmium.     

The role of vitamin E or clay in growing Japanese quail fed diets polluted by cadmium at various levels

This study was conducted to verify whether vitamin (Vit) E or natural clay as feed additives has the potential to modulate the deleterious effects resulting from exposure to cadmium (Cd) in growing Japanese quail. 648 Japanese quail chicks (1 week old) were used to evaluate the effects of dietary Cd (0, 40, 80 and 120 mg/kg diet) and two levels of Vit E (0, 250 mg/kg diet) or two levels of natural clay (0 and 100 mg/kg diet) to study the influences of Cd, Vit E, clay or their different combinations on growth performance, carcass traits, some blood biochemical components and Cd residues in muscles and liver. Live BW and weight gain of quails were linearly decreased with increasing dietary Cd levels. Moreover, feed conversion was significantly worsened with increasing Cd level. Mortality percentage was linearly increased as dietary Cd level increased up to 120 mg/kg diet. Carcass percentage was linearly decreased as dietary Cd level increased. While, giblets percentage were linearly and quadratically differed as dietary Cd level increased. Cd caused significant changes in total plasma protein, albumin, globulin, A/G ratio, creatinine, urea-N and uric acid concentrations as well as ALT, AST and ALP activities. Increasing dietary Cd level was associated with its increase in the muscles and liver. Dietary supplementation with 250 mg of Vit E/kg diet or 100 mg clay/kg improved live BW, BW gain and feed conversion when compared with the un-supplemented diet. Quails fed diet contained 250 mg Vit E/kg and those fed 100 mg clay/kg had the highest percentages of carcass and dressing than those fed the un-supplemented diet. Blood plasma biochemical components studied were better when birds received 250 mg of Vit E/kg diet and those received 100 mg clay/kg. Cd residues in the muscles and liver were significantly less in the birds had 250 mg of Vit E/kg or those received 100 mg clay/kg diet than those un-supplemented with Vit E. Growth performance traits and blood plasma biochemical components studied were significantly affected linearly by the interactions among Cd and each of Vit E and clay levels. In conclusion, the present results indicate that the deleterious effects induced by Cd plays a role in decreasing the performance of Japanese quail and that dietary supplementation with natural clay or Vit E may be useful in partly alleviating the adverse effects of Cd.     

Influence of cadmium on the distribution of the essential trace elements zinc and copper in the liver and kidneys of rats

Cd induced changes of Zn and Cd distribution in the liver and kidneys were studied in relation to Cd metallothionein (MT) synthesis. Wistar male rats were given CdCl₂ by sc injection of .8, 1.5, and 3.0 mg Cd/kg three times a week for three weeks. Cd levels of liver and kidneys increased with the increment of Cd dosage and 80–90% of Cd was found in the cytosol. The MT fractions contained 80–89% cytosolic Cd in the liver and 55–75% Cd in the kidneys. Zn concentrations in the liver increased following Cd administration, But Zn in the kidneys showed only slight increase. There was a distinct decrease of Cu concentration in the liver of the 3.0 mg group. In contrast, Cu concentrations in the kidneys increased about three times in the .8 and 1.5 mg Cd groups, but Cu in the 3.0 mg group showed only 1.5 times increase. The changes of these metal concentrations were observed mainly in the cytosol. Non-MT-Cd in the kidneys was maximum in the 1.5 mg group, but the 3.0 mg group showed significant decrease. In parallel with this decrease of Cd, Cu and Zn in the kidneys showed similar decrease. When the kidneys are injured, Zn and Cu appear to leak from this organ.     

Dietary cadmium decreases lipid peroxidation in the liver and kidneys of the bank vole (Clethrionomys glareolus).

The effect of elevated levels of dietary cadmium on lipid peroxidation in the liver and kidneys of a small rodent, the bank vole, was determined in the present study. Males and females, aged 1 month, were given diets containing 0.40 and 80 mg Cd per kg; liver and kidneys were removed for TBA-RS as well as iron, copper, zinc, cadmium and metallothionein analyses at the end of 6 weeks. Dietary Cd significantly decreased the TBA-RS level in the liver and kidneys of both sexes; however, this effect appeared to be dose-dependent only for the male liver. The changes in hepatic and renal TBA-RS paralleled closely those of tissue iron. Copper concentration decreased significantly only in the male liver, while hepatic and renal zinc were not influenced by dietary Cd. The concentrations of Cd and metallothionein in the liver and kidneys increased significantly in a dose-dependent fashion. Regression analysis confirmed that TBA-RS in both organs correlated closely with iron. The data suggest that dietary Cd decreases hepatic and renal lipid peroxidation indirectly, through lowering the tissue iron concentration.     

4-Vinylcyclohexene diepoxide disrupts sperm characteristics,endocrine balance and redox status in testes and epididymis of rats

Objectives: Exposure to 4-vinylcyclohexene diepoxide (VCD) was reported to induce testicular germ cell toxicity in rodents. However, there is paucity of information on the precise biochemical and molecular mechanisms of VCD-induced male reproductive toxicity.

Methodology: This study investigated the influence of VCD on testicular and epidydimal functions following oral exposure of Wistar rats to VCD at 0, 100, 250 and 500?mg/kg for 28 consecutive days.

Results: Administration of VCD significantly decreased the body weight gain and organo-somatic indices of the testes and epididymis. When compared with the control, VCD significantly decreased superoxide dismutase and catalase activities in the testes whereas it significantly decreased superoxide dismutase activity but increased catalase activity in the epididymis. Moreover, while glutathione peroxidase activity and glutathione level remain unaffected, exposure of rats to VCD significantly increased glutathione S-transferase activity as well as hydrogen peroxide and malondialdehyde levels in testes and epididymis of the treated rats. The spermiogram of VCD-treated rats showed significant decrease in epididymal sperm count, sperm progressive motility, testicular sperm number and daily sperm production when compared with the control. Administration of VCD significantly decreased circulatory concentrations of follicle-stimulating hormone, luteinizing hormone and testosterone along with testicular and epididymal degeneration in the treated rats. Immunohistochemical analysis showed significantly increased cyclooxygenase-2, inducible nitric oxide synthase, caspase-9 and caspase-3 protein expressions in the testes of VCD-treated rats.

Conclusion: Exposure to VCD induces testicular and epidydimal dysfunctions via endocrine suppression, disruption of antioxidant enzymes activities, increase in biomarkers of oxidative stress, inflammation and apoptosis in rats.