Hepatic mitochondrial prooxidant and antioxidant status in ethanol-induced liver injury in rats

In this study, prooxidant and antioxidant status in liver homogenates and their mitochondrial fractions were investigated in both chronic and chronic plus acute ethanol-treated rats. Increases in serum transaminase activities, as well as increases in total lipid, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels and decreases in glutathione (GSH), vitamin E and vitamin C levels, have been observed in liver homogenates following chronic ethanol treatment (20% ethanol, v/v as drinking water for 3 months), but CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities remained unchanged in postmitochondrial fractions. When an acute dose of ethanol (5 g/kg, i.p.) was given rats which had received ethanol chronically, serum transaminase activities and hepatic lipid and MDA and DC levels increased further, but GSH levels and antioxidant enzymes decreased more compared to the chronic ethanol-treated rats. There were no significant differences in the levels of MDA, DC and protein carbonyl and the activities of GSH-Px and GST in the hepatic mitochondrial fraction of rats following both chronic and chronic plus acute treatments. Mn-superoxide dismutase (MnSOD) activities increased in both groups, but mitochondrial GSH levels decreased only after chronic plus acute treatment. Therefore, we suggest that the increase in MnSOD activity may play an important role in the regulation of mitochondrial susceptibility against ethanol-induced oxidative stress.     

Effect of wastewater intake on antioxidant and marker enzymes of tissue damage in rat tissues: Implications for the use of biochemical markers

In the present study, alteration in antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) and marker enzymes of tissue damage alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) with laboratory exposure to wastewaters from Aligarh (AWW) and Saharanpur (SWW) were investigated in rat liver and kidney. Levels of malondialdehyde (MDA), reduced glutathione (GSH) and hydrogen peroxide (H₂O₂) were also determined.A profound enhancement of 5 and 2.5-folds in MDA level was recorded in the liver and kidney respectively as a result of oral administration of SWW to the rats. Exposure to both AWW and SWW resulted in 3–4-fold increase in GR activity and 3-fold increase in SOD and ALT activity in the hepatic tissue compared to control values. Ingestion of AWW and SWW resulted in 3.5-fold rise in renal AST levels whereas AWW caused 75% decline in GST activity in kidney of treated rats.Results indicate that wastewater (AWW/SWW) caused severe damage to renal and hepatic tissues and the effect seems in part to be mediated by suppression of antioxidant system with GR and SOD as potential candidates for hepatic toxicity biomarkers of wastewaters.     

l-Theanine prevents alcoholic liver injury through enhancing the antioxidant capability of hepatocytes

l-Theanine is a unique amino acid in green tea. We here evaluated the protective effects of l-theanine on ethanol-induced liver injury in vitro and in vivo. Our results revealed that l-theanine significantly protected hepatocytes against ethanol-induced cell cytotoxicity which displayed by decrease of viability and increase of LDH and AST. Furthermore, the experiments of DAPI staining, pro-caspase3 level and PARP cleavage determination indicated that l-theanine inhibited ethanol-induced L02 cell apoptosis. Mechanically, l-theanine inhibited loss of mitochondrial membrane potential and prevented cytochrome c release from mitochondria in ethanol-treated L02 cells. l-Theanine also prevented ethanol-triggered ROS and MDA generation in L02 cells. l-Theanine restored the antioxidant capability of hepatocytes including GSH content and SOD activity which were reduced by ethanol. In vivo experiments showed that l-theanine significantly inhibited ethanol-stimulated the increase of ALT, AST, TG and MDA in mice. Histopathological examination demonstrated that l-theanine pretreated to mice apparently diminished ethanol-induced fat droplets. In accordance with the in vitro study, l-theanine significantly inhibited ethanol-induced reduction of mouse antioxidant capability which included the activities of SOD, CAT and GR, and level of GSH. These results indicated that l-theanine prevented ethanol-induced liver injury through enhancing hepatocyte antioxidant abilities.     

Selenium modulates β‐cyfluthrin‐induced liver oxidative toxicity in rats

This study was designed to investigate the possibility of β‐cyfluthrin to induce oxidative stress and biochemical perturbations in rat liver and the role of selenium in alleviating its toxic effects. Male Wister rats were randomly divided into four groups of seven each, group I served as control, group II treated with selenium (200 µg/kg BW), group III received β‐cyfluthrin (15 mg/kg BW, 1/25 LD₅₀), and group IV treated with β‐cyfluthrin plus selenium. Rats were orally administered their respective doses daily for 30 days. The administration of β‐cyfluthrin caused elevation in lipid peroxidation (LPO) and reduction in the activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), glutathione S‐transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR). A decrease in reduced glutathione (GSH) content was also observed. Liver aminotransferases (AST and ALT) and alkaline phosphatase (ALP) were decreased, whereas lactate dehydrogenase (LDH) was increased. Selenium in β‐cyfluthrin‐induced liver oxidative injury of the rats modulated LPO, CAT, SOD, GSH, GST, GPx, and GR. Also, liver AST, ALT, ALP, and LDH were maintained near normal level due to selenium treatment. It is concluded that selenium scavenges reactive oxygen species and render a protective effect against β‐cyfluthrin toxicity. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1323–1329, 2014.     

Effect of cigarette smoke inhalation on antioxidant enzymes and lipid peroxidation in the rat

Inhalation of cigarette smoke significantly increased glutathione (GSH) content and increased lipid peroxidation without altering the activities of Superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) or glutathione reductase (GR) in the lung (six male Wistar rats). Following intratracheal administration of benzo[a]pyrene (BP), an increase in pulmonary GSH-Px activity, GSH content and lipid peroxidation was observed after 12 h. GSH-Px activity and GSH content returned to control values by 7 and 30 days, respectively, whereas lipid peroxidation in the lung remained significantly greater than the control value for up to 7 days of BP administration. Hepatic activity of SOD was increased significantly, whereas the activities of GSH-Px, catalase, GR, and GSH content were not changed by inhalation of cigarette smoke. On administration of BP, a significant increase in the activities of SOD and GSH-Px was observed at 12 h. After 7 and 30 days, the activities of these antioxidant enzymes were comparable to their respective control group values. No change in the activity of catalase or in the level of lipid peroxidation was noted throughout the entire study period.     

Changes in antioxidant defense systems induced by thiram in V79 Chinese hamster fibroblasts.

The role of antioxidant defence systems in protection against oxidative damage of lipids and proteins induced by fungicide thiram during in vitro exposure was investigated in cultured Chinese hamster V79 cells with normal, depleted, and elevated glutathione (GSH) levels. We analyzed the catalytic activities of superoxide dismutases (SOD1 and SOD2), Se-dependent and Se-independent glutathione peroxidases (GSH-Px), glutathione reductase (GR), and catalase (CAT), as well as total glutathione/glutathione disulfide ratio (GSH(total)/GSSG). Thiram treatment resulted in an increase in activities of SOD1, Se-dependent GSH-Px, and GR at the highest tested dose (150 microM). On the contrary, inhibition of CAT and Se-independent GSH-Px activities, and no significant changes in the level of SOD2 activity was observed at any tested doses (100-150 microM). GSH(total)/GSSG ratio in the 100 microM thiram treated cells was not significantly changed comparing to the control, despite significant decrease of GSH total (50%). In 150 microM thiram treated cells the ratio falls to 43% of control value. Pretreatment with l-buthionine sulfoximine (L-BSO), an inhibitor of GSH synthesis, significantly enhanced decrease in CAT and Se-independent GSH-Px activities, as well as GSH(total)/GSSG ratio, and reduced Se-dependent GSH-Px activity, following exposure to thiram. Simultaneously, L-BSO pretreatment enhanced increase in SOD1 activity, and had no effect on SOD2, following thiram exposure. Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram. GSH(total)/GSSG ratio was restored to the control value. This study suggests that following the changes in antioxidant defense systems thiram can act through the production of free radicals.     

Antioxidant enzyme activity and lipid peroxidation in liver and kidney of rats exposed to microcystin-LR administered intraperitoneally.

The effect of acute exposure of intraperitoneal injection of microcystin-LR (MCLR) on antioxidant enzymes and lipid peroxidation has been studied in liver and kidney of rats. Rats were treated with two doses, i.e. 100 and 150 microg of pure MCLR/kg body weight or saline solution. The enzyme activities of glutathione peroxidase (GSH-Px), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) in the liver were significantly decreased in MCLR-treated rats. The decrease of GR activity in the liver was 60%, followed by GSH-Px, SOD and CAT. Similarly, a decrease in the antioxidant enzymes was found in the kidney of MCLR-treated rats, such as GSH-Px (27-31%), GR (22%), SOD (42%) and CAT (25-28%). Concomitantly, significant increases in lipid peroxidation levels were recorded in liver (121 and 196% for 100 and 150 microg/kg, respectively) and kidney (48 and 58% for 100 and 150 microg/kg, respectively) from MCLR-treated rats. In conclusion, acute exposure to MCLR results in a decrease in the antioxidant enzymes and an increase in lipid peroxidation in liver and kidney rats, suggesting the oxidative stress as an important role in the pathogenesis of MCLR-induced toxicity. Antioxidant enzymes were significantly consumed in the liver and a minor decrease was found in kidney, confirming the organ-specific effects of MCLR.     

阿魏酸钠对乙醇所致小鼠肝脏抗氧化功能改变的拮抗作用

研究了不同剂量乙醇对小鼠抗氧化和解毒功能的影响以及阿魏酸钠的拮抗作用。结果表明,大剂量乙醇(11.4g·kg^-1ig)引起肝脏GSH-Px活性升高的同时,肝脏GSH-Re,SOD和GST活性降低,GSH耗竭,而血清GST升高;阿魏酸钠(100mg·kg^-1ig,qd×10)预处理则明显拮抗大剂量乙醇所致的上述改变。表明阿魏酸钠对急性乙醇所致肝损害具有良好保护作用,其机理可能与提高GSH氧化还原酶功能、增加SOD活性和增强GSH结合反应有关。研究结果还提示,血清GST水平是反映乙醇性肝损害的灵敏指标。     

地塞米松对双氯芬酸钠肝损伤的保护作用

目的探讨地塞米松(dexamethasone,Dex)对双氯芬酸钠诱导的大鼠药物性肝损伤的保护作用及部分机制。方法大鼠随机分为正常对照组、模型对照组、Dex(10 mg.kg-1)给药组。Dex(10 mg.kg-1)腹腔注射,1 h后腹腔注射双氯芬酸钠100 mg.kg-1,24 h后检测ALT和AST活性、测定肝匀浆中MDA、GSH含量和GSH-Px、SOD活性,观察肝组织病理学变化,并测肝线粒体膜电位、线粒体肿胀度、NADH水平、SDH及ATPase活性。结果模型对照组血清ALT、AST升高,光镜下可见肝小叶内肝细胞片状坏死,肝匀浆MDA含量升高,GSH、GSH-Px和SOD含量降低,肝线粒体NADH含量、SDH及ATPase活性降低。Dex可明显降低ALT、AST活性(P<0.05),减轻肝脏炎症,降低肝匀浆中MDA含量(P<0.01),升高GSH含量、GSH-Px和SOD活性以及线粒体中NADH含量、SDH及ATPase活性(P<0.01)。结论 Dex对双氯芬酸钠诱导的大鼠药物性肝损伤有保护作用,作用机制可能与减轻线粒体损伤有关。     

Protective effect of grape seed proanthocyanidin extract against oxidative stress induced by cisplatin in rats

Cisplatin is one of the most potent chemotherapeutic antitumor drugs. Oxidative stress has been proven to be involved in cisplatin-induced toxicity. Therefore, the present study was undertaken to examine the antioxidant potential of grape seed proanthocyanidin extract (GSPE) against the toxicity of cisplatin in male rats. Cisplatin treated animals revealed a significant elevation in plasma, heart, kidney and liver thiobarbituric acid reactive substances (TBARS), while the activities of antioxidant enzymes (GST, SOD, CAT and GSH-Px, and the levels of glutathione (GSH) were decreased. Aspartate and alanine transaminases (AST and ALT), creatine kinase and lactate dehydrogenase were significantly increased in plasma, while liver AST and ALT were significantly decreased. Cisplatin significantly increased the levels of plasma total lipid, cholesterol, urea and creatinine, and the relative weight of kidney. On the other hand, plasma total protein and albumin, and body weight were significantly decreased. GSPE reduced cisplatin-induced the levels of TBARS in plasma, heart, kidney and liver, TL, cholesterol, urea and creatinine, and liver AST and ALT. Moreover, it ameliorated cisplatin-induced decrease in the activities of antioxidant enzymes, and GSH, total protein and albumin. Therefore, the present results revealed that GSPE exerts a protective effect by antagonizing cisplatin toxicity.     

Some enzymatic/nonenzymatic antioxidants as potential stress biomarkers of trichloroethylene,heavy metal mixture,and ethyl alcohol in rat tissues

Enzymatic and nonenzymatic antioxidants serve as an important biological defense against environmental pollutants. Various enzymatic and nonenzymatic antioxidants as a stress biomarker in liver and kidney of rat were investigated. The antioxidant enzymes that were analyzed included superoxide dismutase (SOD), catalase, glutathione reductase (GR), glutathione‐S‐transferase (GST), and glutathione peroxidase. Levels of lipid peroxidation (LPO), reduced glutathione (GSH), as well as hydrogen peroxide (H₂O₂) were also measured in homogenates of the liver and kidney of the treated animals to determine oxidative stress induced by trichloroethylene (TCE), ethyl alcohol, and heavy metal mixture (H.M.M) individually and in different combinations. An increase up to the extent of 382% in malonaldehyde, a marker of LPO, was recorded in almost all the treatment groups in both the tissues. Similarly, a rise of 218% in GST activity was also recorded in kidney of TCE‐treated animals. Although H.M.M ingestion resulted in significant change of 125% in SOD activity of hepatic tissue, the level of GR was increased by 93% in the renal tissue of the exposed rats. Solitary dose of alcohol in general did not show a significant change. Moreover, the changes in the levels of antioxidants were much more prominent when these toxicants were given in combination rather than alone. Overall, these results demonstrate the changes in the levels of antioxidant enzymes and GSH system, as well as alterations in the LPO and H₂O₂ levels as a result of test toxicants. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2010.     

Amelioration of cyclophosphamide-induced hepatotoxicity by the root extract of Decalepis hamiltonii in mice

Hepatoprotective potential of the aqueous extract of the roots of Decalepis hamiltonii (DHA) against cyclophosphamide (CP)-induced oxidative stress has been investigated in mice. Administration of CP (25 mg/kg b.w., i.p) for 10 days induced hepatic damage as indicated by the serum marker enzymes aspartate and alanine transaminases (AST, ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). Parallel to these changes CP induced oxidative stress in the liver as evident from the increased lipid peroxidation (LPO), reactive oxygen species (ROS), depletion of glutathione (GSH), and reduced activities of the antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST). Treatment with DHA (50 and 100 mg/kg b.w., po) mitigated the CP-induced oxidative stress. Moreover, expression of genes for the antioxidant enzymes, were down-regulated by CP treatment which was reversed by DHA. Our study shows the DHA protected the liver from toxicity induced by CP and therefore, it could be serve as a safe medicinal supplement during cyclophosphamide chemotherapy.     

Nickel induced lipid peroxidation in the rat: correlation with nickel effect on antioxidant defense systems

Lipid peroxidation (LPO) and alterations in cellular systems protecting against oxidative damage were determined in the liver, kidney and skeletal muscle of male F344/NCr rats, 1 h to 3 days after a single intraperitoneal (i.p.) injection of 107 mumol nickel(II)acetate per kg body weight. At 3 h, when tissue nickel concentrations were highest, the following significant (at least, P less than 0.05) effects were observed: in kidney, increased LPO (by 43%), increased renal iron (by 24%), decreased catalase (CAT) and glutathione peroxidase (GSH-Px) activities (both by 15%), decreased glutathione (GSH) concentration (by 20%), decreased glutathione reductase (GSSG-R) activity (by 10%), and increased glutathione-S-transferase (GST) activity (by 44%); the activity of superoxide dismutase (SOD) and gamma-glutamyl transferase (GGT), as well as copper concentration, were not affected. In the liver, nickel effects included increased LPO (by 30%), decreased CAT and GSH-Px activities (both by 15%), decreased GSH level (by 33%), decreased GSSG-R activity (by 10%) and decreased GST activity (by 35%); SOD, GGT, copper, and iron remained unchanged. In muscle, nickel treatment decreased copper content (by 43%) and the SOD activity (by 30%) with no effects on other parameters. In blood, nickel had no effect on CAT and GSH-Px, but increased the activities of alanine-(ALT) and aspartate-(AST) transaminases to 330% and 240% of the background level, respectively. In conclusion, nickel treatment caused profound cell damage as indicated by increased LPO in liver and kidney and leakage of intracellular enzymes, ALT and AST to the blood. The time pattern of the resulting renal and hepatic LPO indicated a possible contribution to its magnitude from an increased concentration of nickel and concurrent inhibition of CAT, GSH-Px and GSSG-R, but not from increased iron or copper levels. The oxidative damage expressed as LPO was highest in the kidney and lowest in the muscle, which concurs with the corresponding ranking of nickel uptake by these tissues.     

Protective effects of Dunaliella salina – A carotenoids-rich alga,against carbon tetrachloride-induced hepatotoxicity in mice

The protective effects of Dunaliella salina (D. salina) on liver damage were evaluated by carbon tetrachloride (CCl₄)-induced hepatotoxicity in mice. Male ICR mice were orally treated with D. salina or silymairn daily with administration of CCl₄ twice a week for 8 weeks. CCl₄ induced liver damage and significantly (p < 0.05) increased the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in serum and decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and GSH content in liver whereas increased hepatic malondialdehyde (MDA) content as compared with control group. Treatment with D. salina or silymarin could significantly (p < 0.05) decrease the ALT, AST, and ALP levels in serum and increase the activities of SOD, catalase, GSH-Px, glutathione reductase, and GSH content and decrease the MDA content in liver when compared with CCl₄-treated group. Liver histopathology also showed that D. salina reduced the incidence of liver lesions induced by CCl₄. The results suggest that D. salina exhibits potent hepatoprotective effects on CCl₄-induced liver damages in mice, and that the hepatoprotective effects of D. salina may be due to both the increase of antioxidant enzymes activities and inhibition of lipid peroxidation.     

Hepatoprotective potentials of Phyllanthus amarus against ethanol-induced oxidative stress in rats

The hepatoprotective effect of methanolic extract of the leaf of Phyllanthus amarus (P. amarus) against ethanol-induced oxidative damage was investigated in adult male Wistar albino rats. P. amarus (250 and 500 mg/kg/day) and ethanol (5 g/kg/day, 20% w/v) were administered orally to animals for 4 weeks and 3 weeks, respectively. Ethanol treatment markedly decreased the level of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the liver, which were significantly enhanced by P. amarus treatment. Glutathione-S transferase (GST), which was increased after chronic ethanol administration, was significantly reduced by P. amarus treatment in the liver. Also, P. amarus significantly increased the activities of hepatic alanine transaminase (ALT) and aspartate transaminase (AST) as well as alkaline phosphatase (ALP), with a concomitant marked reduction in the plasma activity of the transaminases in the ethanol-challenged rats. Lipid peroxidation level, which was increased after chronic ethanol administration, was significantly reduced in the liver by P. amarus co-treatment. Results show that P. amarus leaf extract could protect the liver against ethanol-induced oxidative damage by possibly reducing the rate of lipid peroxidation and increasing the antioxidant defence mechanism in rats.     

Methiocarb-induced oxidative damage following subacute exposure and the protective effects of vitamin E and taurine in rats

Methiocarb, is used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. In this study, we aimed to investigate subacute effects of methiocarb on lipid peroxidation, reduced glutathione (GSH), antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and histopathological changes in rat tissues. Moreover, we examined the possible protective effects of vitamin E and taurine on methiocarb-induced oxidative damage in rat tissues. Rats were randomly divided into six groups as follows; I-control group; II-methiocarb group; III-vitamin E group; IV-vitamin E + methiocarb group; V-taurine group and VI-taurine + methiocarb group. Methiocarb significantly increased lipid peroxidation in liver and kidney when compared to control groups. Levels of GSH and activities of SOD, CAT and GSH-Px were found to be decreased, while GSH-Rd remained unchanged in rat liver and kidney treated with methiocarb. Pretreatment of vitamin E and taurine resulted in a significant decrease on lipid peroxidation, alleviating effects on GSH and antioxidant enzymes. The degenerative histological changes were less in liver than kidney of rats treated with methiocarb. Pretreatment of vitamin E and taurine showed a protective effect on the histological changes in kidney comparing to the liver of rats treated with methiocarb.     

Comparative effects of curcumin and resveratrol on aflatoxin B1-induced liver injury in rats

Aflatoxin B₁ is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B₁-induced toxicity that could be counteracted by antioxidants. Many plant constituents have been reported to prevent liver damage associated with lipid peroxidation. In this study, curcumin (polyphenolic antioxidant purified from turmeric) and resveratrol (polyphenol obtained from grapes) were evaluated for possible protection against liver injury induced by aflatoxin B₁ in rats. Adult male Fischer rats were divided into six groups including untreated control, curcumin control (200 mg/kg BW), resveratrol control (10 mg/kg BW) and aflatoxin B₁ (25 μg/kg BW). Other two groups were administered either curcumin or resveratrol along with aflatoxin B₁. The study was carried out for 90 days. At the end of the experiment period, blood and tissue samples were collected from the animals before they were killed. Livers were collected for histopathologic studies and fixed in 10% buffered formalin solution. Serum was used for estimation of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl transferase (γ-GT) enzymes. The lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated in liver homogenates. The results revealed that aflatoxin B₁ administration caused liver damage as indicated by statistically significant (P < 0.05) increase in serum ALT, AST and γ-GT levels. In addition, there were general statistically significant reductions in the activities of GSH, SOD, CAT, GSH-Px, and an increase in lipid peroxidation in the liver of aflatoxin B₁-treated group compared to the untreated control group. Curcumin showed a significant hepatoprotective activity by lowering the levels of serum marker enzymes, lipid peroxidation and elevating the levels of GSH, SOD, CAT and GSH-Px. However, resveratrol failed to protect from the aflatoxin B₁-induced liver injury. These findings suggest that curcumin but not resveratrol has a hepatoprotective effect against aflatoxin B₁-induced liver injury.     

Evaluation of antioxidant status in liver tissues: effect of iron supplementation in experimental hyperthyroidism

The antioxidant defense system in liver tissue in experimental hyperthyroidism and/or in iron supplementation was investigated. Thyroid hormones (T3, T4, TSH), ferritin (marker of iron status), antioxidant status components (glutathione [GSH], glutathione peroxidase [GSH-Px], superoxide dismutase [SOD]), and serum transaminases (GOT and GPT, both of which are known to be released from damaged hepatocytes), were measured. Hyperthyroidism in rats, induced by L-thyroxine administration, significantly raised SOD activity (p < 0.05), but significantly decreased GSH-Px activity and GSH values (p < 0.001) in the liver. In the L-thyroxine administered and iron supplemented (TI) group, GSH and GSH-Px values of liver tissues were significantly lower than those of control rats (p < 0.05). GSH-Px levels of the TI group were higher (p < 0.001), and SOD levels significantly lower (p < 0.001) than those of the L-thyroxine administered group. We conclude that hyperthyroidism induces SOD activity in liver; ferritin levels increase in hyperthyroidism, contributing to the antioxidant defense system; GSH-Px and GSH levels are decreased significantly in hyperthyroidism either due to inactivation due to increased oxidative stress or to insufficient synthesis; iron supple- and GPT analysis); iron decreases the effect of T4. This must be taken into consideration during iron supplementation.     

Biochemical changes in the rat lung and liver following intratracheal instillation of cadmium oxide

Acute biochemical changes in the rat lung and liver following intratracheal instillation of cadmium oxide (CdO) were observed at a dose of 5 micrograms Cd/rat to investigate the defense mechanism to Cd intoxication via airway. In the lung metallothionein (MT) was induced, reaching a maximum at 2 days. A slight increase in reduced glutathione (GSH) concentration was observed at 4 days. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was increased and superoxide dismutase (SOD) activity was slightly decreased, but glutathione peroxidase (GPx) and glutathione reductase (GR) activities were not changed. These observations suggested that MT played a key role in detoxification of instilled CdO, but that the antioxidant enzymes had a minimal role. In the liver MT and GSH concentrations were diminished 7 h after instillation and returned to their control levels. Hepatic GPx activity was increased 1 day after instillation and the significantly elevated level lasted up to 7 days, while hepatic GR activity was decreased. These hepatic biochemical changes are suggested to be due to the secondary effects of the lung injury.     

The influence of ascorbic acid on nickel-induced hepatic lipid peroxidation in rats.

We studied the effect of oral ascorbic acid treatment on nickel sulfate-induced lipid peroxidation in the liver of Wistar strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were estimated in liver. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased glutathione, SOD, CAT, and GSH-Px activities in liver. The simultaneous administration of ascorbic acid with nickel sulfate resulted in a remarkable improvement of lipid peroxide, glutathione, SOD, CAT, and GSH-Px status in liver in comparison with rats treated with nickel alone. Nickel sulfate has an adverse effect on hepatic lipid peroxidation in animals, but simultaneous treatment with ascorbic acid offers a relative protection against nickel-induced hepatotoxicity.