花青素对大鼠视网膜光化学损伤保护作用

目的 观察黑米皮花青素(BRACs)对视网膜光化学损伤(RPD)的保护效应与抗氧化能力的关系.方法60只SD大鼠随机分为对照组、光照组和BRACs干预组,采用苏木素-伊红染色和透射电镜技术观察视网膜形态结构变化,测定眼眶血中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)活性.结果 光照组大鼠视网膜结构紊乱,MDA含量(8.82 nmoL/mL)和SOD活性(27.08 U/mL)明显高于对照组(P＜0.05),GST活性(24.96 U/mL)低于对照组(P＜0.05);与光照组比较,BRACs干预组视网膜形态结构基本正常,MDA含量(6.85 nmol/mL)下降(P＜0.05),SOD、GSH-Px、GST活性(28.90,433.69,34.75U/mL)升高(P＜0.05).结论 BRACs对大鼠视网膜光化学损伤具有保护作用.     

白桦脂醇对大鼠酒精性肝损伤保护作用

目的 观察白桦脂醇对大鼠酒精性肝损伤的抗氧化作用.方法 将大鼠随机分为6组,正常组、低剂量组、中剂量组、高剂组量、阳性对照组(益肝灵组)和模型组.采用白酒灌胃的方法建立大鼠酒精性肝病模式,给予白桦脂醇保护.测定肝匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽-S-转移酶(GST)活性和还原性谷胱甘肽(GSH)、丙二醛(MDA)含量,同时进行肝脏的病理切片观察.结果 高剂量白桦脂醇组中SOD、GSH-Px和GST活性和GSH含量明显升高,MDA含量明显降低,和模型组比较,差异均有统计学意义(P<0.01或P<0.05).阳性对照组可明显提高酒精性肝损伤大鼠肝组织中SOD、GSH-Px、GST活性和GSH含量,明显降低MDA含量,与模型组比较,差异均有统计学意义(P<0.01或P<0.05).高剂量白桦脂醇还能明显改善由酒精引起的肝组织脂肪样变和坏死.结论 白桦脂醇能抑制酒精诱导脂质过氧化反应对肝组织的损伤,对酒精性肝损伤有明显的保护作用.     

大剂量芹菜素对大鼠抗氧化酶活性及DNA损伤影响的研究

目的观察大剂量芹菜素对大鼠的抗氧化活性及对DNA氧化损伤的影响。方法将100只Wistar大鼠随机分为5组,每组20只,即基础饲料对照组,低剂量芹菜素组(掺入量为2.5%,相当于2g/kgbw),次低剂量芹菜素组(掺入量为5.0%,相当于4g/kgbw),中剂量芹菜素组(掺入量为7.5%,相当于6g/kgbw),高剂量芹菜素组(掺入量为10%,相当于8g/kgbw),实验周期为13周。实验结束前收集动物2h尿液,实验结束后处死动物,留取血液和肝脏,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽硫转移酶(GST)活性、丙二醛(MDA)含量,分析8-羟基脱氧鸟苷含量。结果在2和4g/kgbw剂量时,雄性肝脏SOD、GSH-Px以及2g/kgbw剂量组的GST活性明显低于对照组(P<0.05);血清中雄性8g/kgbw剂量组的GST以及雌雄4g/kgbw剂量组的GSH-Px活性明显低于对照组(P<0.05),其他各项指标与对照组比较,差异均无显著性。结论本试验条件下,大剂量芹菜素能够降低雄性大鼠的抗氧化酶活性,但对DNA损伤没有影响。     

强化SOD刺梨汁对燃煤型砷中毒脂质过氧化损害的拮抗作用

[目的]探讨强化SOD刺梨汁对燃煤型砷中毒患者脂质过氧化作用的影响及其作用机制。[方法]采用生化法分别测定强化SOD刺梨汁、刺梨汁治疗前后患者血中超氧化物歧化酶(superoxidedismutase,SOD)、谷胱甘肽过氧化物酶(glutathioneperoxidase,GSH-PX)及谷胱甘肽硫转移酶(glutathione-s-transferase,GST)的活性,谷胱甘肽(glutathione,GSH)及巯基(hydrosulfidegroup,-SH)含量和丙二醛(malondialdehyde,MDA)水平。[结果]强化SOD刺梨汁治疗后患者的SOD、GSH-PX及GST活力均较治疗前明显升高,GSH及-SH含量显著增加,MDA水平则明显降低(P<0.05或P<0.01);刺梨汁治疗后患者的SOD、GSH-PX及GST活力亦较治疗前显著提高(P<0.05),但GSH-SH含量及MDA水平在治疗前后差异不显著;与刺梨汁治疗组比较,强化SOD刺梨汁组患者的SOD活性及-SH含量显著提高(P<0.05),MDA水平明显降低(P<0.05)。[结论]强化SOD刺梨汁可提高燃煤型砷中毒患者机体抗氧化物质的活性或含量,拮抗砷中毒自由基脂质过氧化的损害作用。强化SOD刺梨汁的作用优于单纯刺梨汁。     

谷胱甘肽和α-硫辛酸对锰致大鼠体内过氧化反应的影响

将Wistar大鼠32只随机分为4组,即对照组、单纯染锰组、硫辛酸(LA)干预组、谷胱甘肽(GSH)干预组。对照组腹腔注射生理盐水,其余各组腹腔注射MnCl2150μmol/kg,2 h后,对照组、单纯染锰组皮下注射生理盐水,每周染毒5次;硫辛酸干预组皮下注射LA 35μmol/kg,谷胱甘肽干预组皮下注射GSH 1 mmol/kg,隔日干预,共计4周。测定肝、脑和肾组织中的谷胱甘肽(GSH)、丙二醛含量(MDA)和谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性。结果与对照组比较,单纯染锰组肝、脑、肾组织中的MDA含量均升高(P<0.05),GSH含量和GSH-Px、SOD的活性都有不同程度的降低;两干预组肾组织中MDA含量降低(P<0.01,P<0.05)。与单纯染锰组比较,GSH干预组肝组织的MDA、GSH含量降低(P<0.05),SOD、GSH-Px活性升高(P<0.05),脑和肾组织的MDA含量降低(P<0.05,P<0.01);LA干预组肝组织SOD、GSH-Px的活性升高(P<0.01),脑、肾组织的MDA含量降低(P<0.05,P<0.01)。提示GSH和LA对锰致大鼠氧化损伤有一定的拮抗作用。     

高氟染毒新西兰白兔某些氧化、抗氧化与血管功能指标的变化

目的观察高氟染毒新西兰白兔某些氧化、抗氧化和血管功能指标的变化。方法 20只雄性新西兰白兔随机分为对照组,饮去离子水,饲基础饲料;高脂组,饮去离子水,饲基础饲料加0.5%胆固醇、7%蛋黄粉高脂饲料;高氟组,饮含氟质量浓度100mg/L高氟水,饲基础饲料;高氟高脂组,饮含氟质量浓度100mg/L高氟水,饲基础饲料加0.5%胆固醇、7%蛋黄粉高脂饲料,实验期6个月。于实验前、实验3个月、6个月取血氟离子电极法测血氟含量。实验6个月取血、心和肝制备组织匀浆,生化法检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)水平;放免法检测血浆6-酮-前列腺F1α(6-keto-PGFlα)、血栓素B2(TXB2)和内皮素-1(ET-1);生化法检测血清一氧化氮合酶(NOS)、诱导型NOS(iNOS)、内皮型NOS(eNOS)活性;原位杂交法检测白细胞iNOS-mRNA和eNOS-mRNA表达。结果新西兰白兔饮用高氟水3个月、6个月时血清氟升高;6个月时血液、肝和心肌SOD、GSH-Px活性降低(P<0.01,P<0.05)、心肌MDA含量升高(P<0.05);血浆6-keto-PGFlα含量下降(P<0.01),TXB2和ET-1含量升高(P<0.01,P<0.05);血清总NOS活性下降(P<0.05),肝总NOS活力、心肌和肝iNOS活性升高(P<0.05);血白细胞iNOS-mRNA表达增强,eNOS-mRNA表达减弱(P<0.05)。析因方差分析,血清、肝和心肌SOD活性及血清MDA含量,血浆ET-1含量以及血清iNOS活性、肝总NOS活性等指标高氟与高脂具有交互增强作用(P<0.01,P<0.05)。结论高氟抑制抗氧化酶,血管内皮功能受损,机体NO代谢紊乱,此过程高氟与高脂具有一定的协同作用。     

银杏叶提取物对酒精所致大鼠睾丸氧化损伤的保护作用的研究

目的研究银杏叶提取物(EGB)对酒精所致大鼠睾丸氧化损伤的预防保护作用。方法雄性SD大鼠30%酒精灌胃(2.37g/kgbw)前,EGB采用分组(低剂量组48μg/gbw和高剂量组96μg/gbw)预防性给药的方法。于实验90d检测大鼠睾丸组织中超氧化物歧化酶(SOD)、谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、和谷胱甘肽(GSH)、活性氧(ROS)以及丙二醛(MDA)的含量。通过亚细胞分离方法提取大鼠睾丸微粒体,测定微粒体血红素氧化酶-1(HO-1)活性。采用RT-PCR检测睾丸组织中血红素氧化酶-1(HO-1)mRNA表达水平。结果慢性酒精摄入90d后,EGB组睾丸匀浆ROS、MDA较酒精组有明显降低(P<0.05);相反,GST、G-Px、CAT、SOD、HO-1活性以及GSH均有显著性升高(P<0.05);EGB诱导HO-1高表达。结论长期慢性酒精摄入引起大鼠睾丸氧化损伤。EGB可作为一种预防性的抗氧化剂减轻这种氧化损伤;其机制可能与诱导HO-1高表达,清除自由基,抑制脂质过氧化反应有关。     

银杏叶提取物预防大鼠酒精性肝损伤的机制研究

目的:观察银杏叶提取物(EGB)对大鼠酒精性肝损伤的预防作用,并研究其可能的分子机制。方法:无水乙醇灌胃13w,EGB采用预防性给药的方法,检测大鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)活性;肝组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和谷胱甘肽(GSH)、丙二醛(MDA)的含量;采用RT-PCR检测肝组织中血红素氧化酶-1(HO-1)mRNA表达水平。结果:与酒精组相比,EGB组ALT、AST活性均显著降低(P<0.05),MDA含量非常显著降低(P<0.01);SOD、GSH-Px活性和GSH含量较酒精组均显著升高(P<0.05);此外,EGB可以诱导HO-1mRNA高表达。结论:EGB通过减少酒精所致GSH的耗竭,增加抗氧化物质活性或含量,抑制脂质过氧化反应从而预防酒精性肝损伤,其机制可能与诱导HO-1表达有关。     

金属镉作业人群的脂质过氧化与抗氧化能力的观察

目的 观察金属镉接触作业人群体内的脂质过氧化产物和抗氧化酶的变化。方法 选取91名接触金属镉（Cd）的作业人员为接触组，并以79名不接触任何毒物的健康人作为对照组，测定血清中丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽硫转移酶（GST）。结果 接触组的SOD、GSH-Px和GST的活性明显下降，而MDA明显增高（P〈0．05）。以工龄分组比较，显示长工龄组较短工龄组MDA高，SOD、GSH-Px和GST活性低（P〈0．05）。结论 Cd能增加体内脂质过氧化产物含量，降低机体的抗氧化能力，增加职业接触人群对氧化应激的易感性。     

PARP抑制剂对早期糖尿病大鼠肾脏的保护作用

目的观察短期应用PARP抑制剂3-氨基苯甲酰胺(3-AB)对早期糖尿病大鼠肾脏的保护作用。方法实验动物分为糖尿病对照组(DC组)、糖尿病3-AB治疗组(DT组)、正常对照组(NC组),4周后比较各组血糖、24 h尿蛋白、肌酐清除率(Ccr)、肾重/体重和肾脏丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)含量,免疫组化观察各组大鼠PARP阳性细胞表达。结果和DC组相比,3-AB降低了DT组大鼠尿蛋白、Ccr、肾重/体重、MDA含量(P<0.05),而抗氧化酶SOD、GSH-Px活性则升高(P<0.05),明显降低了DT组PARP阳性细胞数(P<0.01)。结论短期应用3-AB对于糖尿病状态下肾脏内氧自由基代谢具有调节作用,对早期糖尿病大鼠肾脏具有保护作用。     

Melatonin improved the disturbances in hepatic prooxidant and antioxidant balance and hepatotoxicity induced by a high cholesterol diet in C57BL/6J mice

We examined the effect of melatonin in prooxidant and antioxidant state in the liver of C57BL/6J mice fed on a high cholesterol (HC) diet. Mice were fed with normal mice chow containing 1.5% cholesterol and 0.5% cholic acid for 4 months without and with melatonin (10 mg/L in drinking water) treatment. HC diet was observed to increase malondialdehyde (MDA) and diene conjugate (DC) levels in the liver. This diet lowered glutathione (GSH), alpha-tocopherol, and total ascorbic acid levels as well as glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver, but hepatic superoxide dismutase (SOD) activity remained unchanged. Although melatonin treatment did not affect these parameters in mice fed a normal diet, it reduced hepatic MDA and DC levels in mice fed an HC diet. Hepatic alpha-tocopherol and ascorbic acid levels increased, but hepatic GSH levels remained unchanged in the melatonin-treated HC group as compared to the HC group. Melatonin treatment was found to increase liver GSH-Px and GST activities in mice fed an HC diet. However, SOD activity did not alter in the liver of hypercholesterolemic mice following melatonin treatment. In addition, the histopathological lesions observed in the cholesterol-plus-melatonin group were less severe than those seen in the cholesterol group. According to these observations, we can say that melatonin treatment has an ameliorating effect on the disturbances in prooxidant and antioxidant balance and histopathological lesions in the liver of mice following cholesterol feeding.     

Dietary taurine reduces retinal damage produced by photochemical stress via antioxidant and anti-apoptotic mechanisms in Sprague-Dawley rats

Taurine has been shown to be tissue protective in many models of oxidant-induced injury. However, its protective role against retinal damage induced by photochemical stress is less well known. The purpose of the present study was to investigate whether dietary taurine reduced retinal photochemical damage in Sprague-Dawley rats and to further explore the underlying molecular mechanisms of this action. Twenty rats fed AIN-93 formulation and maintained in the dark for 48 h were used as controls (n 20). Another forty rats were randomly divided into two groups and then treated with (n 20) or without 4 % taurine (n 20) for 15 d respectively. After treatment, these two groups were exposed to fluorescent light (3000 +/- 200 lux and 25 degrees C), and the protective effects of dietary taurine were then evaluated. The present results showed that dietary taurine effectively prevented retinal photochemical damage as assessed by changes of morphology. Also, the supplementation caused an increase of taurine in the retina, a decrease of malondialdehyde (P < 0.01), and elevation of superoxide dismutase (P < 0.01) and glutathione peroxidase activities in the retina (P < 0.01). Moreover, dietary taurine inhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P < 0.05), up regulated NF-kappaB (p65) expression (P < 0.05), and decreased caspase-1 expression (P < 0.05) so as to reduce the apoptosis of photoreceptors in the retina (P < 0.05). These results suggest that dietary taurine reduced retinal damage produced by photochemical stress via antioxidant and anti-AP-1-NF-kappaB-caspase-1 apoptotic mechanisms in rats.     

Acute effects of fenthion on certain oxidative stress biomarkers in various tissues of frogs (Rana ridibunda)

This study was aimed mainly to assess the effects of fenthion on certain oxidative stress biomarkers in various tissues of frogs (Rana ridibunda). Biomarkers selected for stress monitoring were malondialdehyde (MDA) and antioxidant defense system (ADS) such as reduced glutathione (GSH) level, glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities in the liver, kidney, heart, and brain of frogs exposed to 10 and 20 ppm dosages of fenthion for 24, 48, 72, and 96 h. The results demonstrate an increase in MDA levels in selected tissues following exposure to both concentrations of fenthion. The ADS, GSH-Px, GST, SOD activities and GSH levels also fluctuated after 24, 48, 72, and 96 h in all the treatment groups compared with controls. From the evidence obtained here, it is concluded that the exposure of frogs to fenthion induced an increase in MDA combined with fluctuated ADS. This may reflect the potential role of these parameters as useful biomarkers for oxidative stress in amphibian species.     

固井水泥粉尘对接触工人抗氧化酶的影响

目的探讨固井水泥粉尘对作业工人和机体脂质过氧化(LPO)的影响.方法对98名固井水泥粉尘接触工人和30名不接尘健康对照进行血清丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性测定.结果与对照组比较,固井水泥粉尘接触工人血清MDA含量升高,SOD和GSH-Px活性下降,差异均有显著性(P＜0.01);相关分析显示:随着作业工人接尘工龄的延长,血清MDA含量有增高的趋势(r=0.357 0, P＜0.01),血清SOD和全血GSH-Px活性呈下降趋势(r=-0.739 8;-0.301 3, P＜0.01).结论固井水泥粉尘作业工人体内氧自由基反应加剧,氧化/抗氧化状态严重失衡.     

EFFECTS OF ENDURANCE TRAINING ON ANTIOXIDANT DEFENSE MECHANISMS AND LIPID PEROXIDATION IN TESTIS OF RATS

Male rats were equally divided into trained rest (TR), trained exhaustive exercise (TE), untrained rest (UR), and untrained exhaustive exercise (UE). Endurance training consisted of treadmill running for 1.5 h/d, 5 days a week for 8 weeks reaching the speed of 2.1 km/h at the fortieth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km/h at 95th min, 10% uphill, continued until exhaustion. Testicular tissue malondialdehyde (MDA), antioxidant potential (AOP) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), glutathione reductase (GR) and catalase (CAT) activities were determined. There was a slight decrease, but not significant, in the SOD activity in UE group compared to TE and TR groups. Activity of GSH-Px decreased in the UE group compared to UR, TR and TE groups. Acute exhaustive exercise did not affect testicular tissue GSH-Px activity in trained rats. Testicular tissue GST activity of the UE group was similar to TE group, but lower than UR and TR groups. In UE group, testicular tissue AOP values were lower than UR, TR and TE groups. The oxidative effects of acute exhaustive exercise on the rat testis decreased with endurance training. Endurance training prevents oxidative injuries by eliminating oxygen radicals and inhibiting lipid peroxidation via preventing decreases in antioxidant enzyme activities.     

番茄红素对小鼠前胃癌的保护作用

目的:观察番茄红素对小鼠前胃组织癌变过程的影响及其作用机制。方法:昆明小鼠随机分成4组,番茄红素组分别饲喂高、中、低不同剂量的番茄红素饲料,模型组饲喂正常饲料,2周后灌喂含苯并(a)芘的色拉油,24周后处死全部动物,观察小鼠前胃癌形成情况,测定血清超氧化物歧化酶(SOD)、过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSH-Px)活性、总抗氧化活力(T-AOC)、丙二醛(MDA)和还原型谷胱甘肽(GSH)含量。结果:与模型组相比,番茄红素高剂量组成瘤率和瘤直径显著减小,MDA含量降低,CAT、GSH-Px活力明显升高,高、中剂量组SOD、T-AOC活性升高。结论:番茄红素具有抑制肿瘤生长的作用,其作用机制可能与提高抗氧化酶活力,降低脂质过氧化产物有关。     

Liver antioxidant defenses in mice fed ethanol and the AIN-76A diet

The effects of chronic alcohol (EtOH) ingestion on antioxidant defenses in mice fed AIN-76A liquid diets were investigated. C57B1/6 female mice were divided into three groups and fed the AIN-76A liquid EtOH diet containing EtOH to provide 31% of total caloric intake (TCI), the same basic diet containing EtOH to provide 35% of TCI, or an isocaloric AIN-76A liquid control diet. After 3 weeks, the mice were killed and livers were excised for biochemical analysis. Liver reduced glutathione (GSH) levels, and activities of both Mn-Superoxide dismutase (SOD) and Cu/Zn-SOD were significantly decreased by both levels of EtOH. Activities of catalase and glutathione transferase (GT) were significantly increased, whereas glutathione peroxidase (GP) activity was not affected by either level of EtOH. Our previous study using the Lieber-DeCarli liquid EtOH diet caused a decline of total SOD and GP activities. The results suggest that chronic EtOH administration decreases liver antioxidant defenses; however, the mice fed the AIN-76A EtOH liquid diet can maintain a higher antioxidant defense capability than those fed Lieber-DeCarli EtOH liquid diet.     

Iron intake affects lipid peroxidation and glutathione peroxidase activity of distal colonic mucosa

The purpose of this study was to examine the effect of low, adequate, and high dietary iron (Fe) levels on lipid peroxidation, glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) activities, and glutathione (GSH) concentrations in colon and liver. Male Sprague Dawley rats were fed iron deficient (DFe; 14 mg Fe/kg diet; N=8), adequate iron (AFe; 39 mg Fe/kg diet, N=8), or high iron (HFe; 454 mg Fe/kg diet; N=8) diets for 3 weeks. Liver Fe concentrations were 26, 84, and 243 ug/g wet weight, respectively, for rats fed DFe, AFe, and HFe diets (p<0.0001). Lipid peroxidation was increased 70% in distal colonic mucosa of rats fed HFe diets compared to that of rats fed AFe and DFe diets (p<0.01), but lipid peroxidation was unaffected by diet in proximal colon or liver. While distal colonic mucosal GSH-Px activity was lower in DFe rats (0.062 U/mg protein), than in AFe rats (0.091 U/mg protein), and HFe rats (0.089 U/mg protein) (p<0.05), iron intake had no effect on GSH-Px activity in proximal colon or liver. The distal colon had higher GSH-Px activity than proximal colon (p<0.0001). GST activity in colon and liver, and hepatic GSH concentrations were not altered by dietary iron intakes. This study suggests that distal and proximal colonic mucosa may respond differently to changes in Fe status.     

Vitamin B-6 deficiency suppresses the hepatic transsulfuration pathway but increases glutathione concentration in rats fed AIN-76A or AIN-93G diets

The transsulfuration pathway, which aids in regulating homocysteine concentration and mediates cysteine synthesis, may be sensitive to vitamin B-6 status because cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CGL) require pyridoxal 5'-phosphate (PLP). To assess relations between vitamin B-6 and transsulfuration, we evaluated the effects of dietary pyridoxine (PN) on the hepatic concentration of relevant metabolites and in vitro activity of CBS and CGL. Growing rats were fed AIN-93G- or AIN-76A-based diets that ranged from adequate to deficient in vitamin B-6 (2, 1, 0.5, 0.1, or 0 mg of PN/kg diet, n = 5). This design allowed assessment of the effects of supplemental methionine (AIN-76A) vs. cysteine (AIN-93G) in common research diets over a range of vitamin B-6 levels. CBS activity, assayed in the presence or absence of added S-adenosylmethionine, was independent of diet type and PN level. CGL activity was independent of diet type but proportional to dietary PN. Rats fed deficient (0 and 0.1 mg PN/kg) diets exhibited only approximately 30% of the CGL activity of those fed the 2 mg PN/kg diets. Hepatic cystathionine increased from 20 to 30 nmol/g for the 1-2 mg PN/kg diets to approximately 85 nmol/g for the 0 mg PN/kg diet; however, cysteine was reduced only in B-6-deficient rats consuming the AIN-93G diet (means of 30-40 nmol/g for adequate to 11.6 nmol/g for 0 mg PN/kg AIN-76A diet). In spite of these effects, hepatic glutathione concentration increased in vitamin B-6 deficiency. These results suggest that vitamin B-6-dependent changes in transsulfuration do not limit hepatic glutathione production.