Dantrolene may prevent organophosphate-induced oxidative stress and muscle injury

The effects of dantrolene against fenthion-induced oxidative stress and muscle injury were investigated in rats. Malondialdehyde (MDA), reduced glutathione (GSH) ascorbic acid, retinol and β-carotene levels in blood were measured. Histopathological alterations and apoptosis in diaphragm were examined. Fenthion increased the level of MDA and decreased the levels of GSH in blood. Dantrolene administration prevented the rise in MDA levels and increased the GSH levels. There was no significant difference between β-carotene levels of experimental groups. However, fenthion toxicity led to decrease in ascorbic acid and retinol levels, dantrolene administration significantly prevented this decrease. Dantrolene significantly decreased the inflammation, edema and muscle necrosis or apoptosis in diaphragm muscle. Results of present study showed that toxicity of organophosphate compound fenthion increases the lipid peroxidation and depresses endogenous antioxidative systems, and leads to muscle injury in organism. Again, dantrolene administration prevents lipid peroxidation, augments antioxidant activity, and decreases muscle injury and apoptosis.     

Protective roles of vitamin E (α-tocopherol), selenium and vitamin E plus selenium in organophosphate toxicity in vivo: A comparative study

In the present study, we investigated the possible protective role of vitamin E, selenium (Se) and vitamin E plus Se in fenthion-induced organophosphates (OP) toxicity in rats. Serum concentrations of ascorbic acid, retinol, β-carotene, ceruloplasmin, nitrite and nitrate as well as levels of malondialdehyde (MDA) and reduced glutathion (GSH) in whole blood and in some tissues such as brain, heart, jejunum, kidney, liver, lung, muscle and pancreas were measured in sham, control, vitamin E, Se and vitamin E + Se groups. Compare to the sham group, the MDA (p < 0.001) and GSH (p < 0.01) levels in whole blood and some in tissues were significantly higher in the control animals. Ceruloplasmin levels of the control (p < 0.05), vitamin E (p < 0.05) and vitamin E + Se (p < 0.01), groups were higher than the sham group. Ascorbic acid, retinol, β-carotene as well as nitrite and nitrate levels in the control group were significantly lower than sham, vitamin E, Se and vitamin E + Se groups. We concluded that fenthion toxicity-induced lipid peroxidation and generation of free radicals in whole blood and tissues. Additionally, the antioxidants we tested did show a significant protective effect against OP-induced tissue and blood injury at the biochemical level.     

Fenthion induced-oxidative stress in the liver of adult rats and their progeny: Alleviation by Artemisia campestris

Fenthion (FEN) is an organophosphate insecticide used in both agricultural and urban areas throughout the world including Tunisia. Recent investigations have proved the crucial role of natural antioxidants to prevent the damage caused by toxic compounds. In this study, we investigated the role of Artemisia campestris (Ac) leaf powder in protection against oxidative damage and hepatotoxicity induced by fenthion in female rats and their pups. Female Wistar rats were divided into four groups: group I served as controls which received standard diet, group II received orally FEN 551 ppm, group III received both 551 ppm of FEN and experimental diet (5% Artemisia) and group IV received experimental diet (5% Artemisia). Oral administration 551 ppm of FEN by drinking water to adult rats caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases and lactate dehydrogenase), total cholesterol (TC) and triglycerides (TG), as well as hepatic malondialdehyde (MDA) levels thus causing a drastic alteration in antioxidant defence system. Particularly, the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) and the level of reduced glutathione (GSH) increased by FEN. These biochemical alterations were accompanied by histological changes marked by leucocytes infiltration, sinusoidal dilatation (moderate peliosis), granuloma inflammatory disorders and necrosis in hepatocytes of dams. While, slight leucocytes infiltration was shown in pups. Treatment with Ac prevented the liver damage induced by FEN, as revealed by inhibition of hepatic lipid peroxidation accompanied by an improvement of liver histopathological changes, CAT and GPx activities except GSH and SOD which were not modified. It could be concluded that A. campestris is promising a protective agent against hepatotoxicity during the exposure to fenthion.     

梨叶片感染轮纹病菌后的生理变化

梨叶片被轮纹病菌感染后,多酚氧化酶(PPO)、过氧化氢酶(CAT)、过氧化物酶(POD)和超氧化物歧化酶(SOD)的活性均显著下降。但叶片内丙二醛(MDA)含量和超氧阴离子(O₂-)的产生速率上升;还原型谷胱甘肽(GSH)和抗坏血酸(ASA)含量降低。这些结果表明,梨叶片被轮纹病菌感染后,叶内活性氧消除系统被破坏,而叶内膜脂过氧化作用加强是最终导致梨叶片受害的原因。     

Effects of N-acetylcysteine on oxidative responses in the liver of fenthion exposed Cyprinus carpio

The aim of this study was to evaluate the effects of different N-acetylcysteine doses on the tolerance to fenthion-induced oxidative stress, alterations in glutathione metabolism and cholinesterase specific activities in the liver by using freshwater fish Cyprinus carpio (Cyprinidae) as a model organism. An acute toxicity study was carried out to determine 96-h median lethal concentration of fenthion for this species (2.16 mg/L) and 80% of this concentration was applied in toxicity studies. Four groups, each containing eight fish were constituted as follows: Control group, fenthion treated group, 0.5 or 400 mg/kg NAC-injected + fenthion-treated groups. Biochemical analyses were carried out spectrophotometrically. Fenthion treatment significantly decreased total glutathione and glutathione levels, glutathione/glutathione disulfide ratio together with glutathione reductase and γ-glutamylcysteine synthetase specific enzyme activities. The higher dose of N-acetylcysteine increased the toxic effects of fenthion and γ-glutamyl transpeptidase specific activity while decreasing glutathione S-transferase specific activity. However, injection of the lower dose provided a limited protection against fenthion toxicity. In all exposure groups, lipid peroxidation increased and total protein levels decreased, while protein depletion was prevented by low dose of N-acetylcysteine application. Acetylcholinesterase and butyrylcholinesterase activities were at similar levels in the liver of C. carpio. A dose-dependent inhibition was observed in butyrylcholinesterase activity by N-acetylcysteine application. The results showed that fenthion had a significant oxidative stress inducing potential through the reduction of glutathione redox capacity. The critical point for overcoming oxidative stress by N-acetylcysteine in fenthion toxicity was the selection of the dose; N-acetylcysteine exerted its toxic effects by means of oxidative stress in fish liver at the higher dose.     

Ameliorative effect of lycopene on antioxidant status in Cyprinus carpio during pyrethroid deltamethrin exposure

The aim of the present study was to investigate the ameliorative properties of lycopene against the toxic effects of deltamethrin (DM) by examining oxidative damage markers such as lipid peroxidation and the antioxidant defense system components in carp (Cyprinus carpio). The fish were divided into seven groups of 15 fish each and received the following treatments: Group 1, no treatment; Group 2, orally administered corn oil; Group 3, oral lycopene (10 mg/kg body weight); Group 4, exposure to 0.018 μg/L DM; Group 5, exposure to 0.018 μg/L DM plus oral administration of 10 mg/kg lycopene; Group 6, exposure to 0.036 μg/L DM; and Group 7, exposure to 0.036 μg/L DM plus oral administration of 10 mg/kg lycopene. Treatment was continued for 14 days, and at the end of this period, blood and tissue (liver, kidney, and gill) samples were collected. Levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were determined in blood and tissues for measurement of oxidant-antioxidant status. A significant elevation in the level of MDA, as an index of lipid peroxidation, and reductions in antioxidant enzyme activities (SOD, CAT, and GSH-Px) and low molecular weight antioxidant (GSH) levels were observed in DM-exposed fish. Treatment with lycopene attenuated the DM-induced oxidative stress by significantly decreasing the levels of MDA. In addition, lycopene significantly increased the SOD, CAT, and GSH-Px activities and the level of GSH. The present results suggest that administration of lycopene might alleviate DM-induced oxidative stress.     

Determination of toxicity of trichloroacetic acid in rats: 50 days drinking water study

This study aims to investigate the effects of the trichloroacetic acid (TCA) on serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation content (Malondialdehyde, MDA) in various tissues of rats. TCA (2000 ppm) as drinking water was administered orally to rats (Sprague-Dawley albino) ad libitum for 50 days continuously. TCA treatments caused different effects on the serum marker enzymes, antioxidant defense systems and the MDA content in experimented rats compared to controls. Results showed that TCA caused a significant increase in serum AST, ALT, CPK and ACP activity. The lipid peroxidation end product MDA slightly increased in the erythrocytes, liver and kidney of rats treated with TCA, whereas did not change in the brain. In addition, antioxidant enzyme activity such as CAT and SOD significantly increased in the brain, liver and kidney tissues of TCA induced group whereas the ancillary enzyme GR and the drug metabolizing enzyme GST activity did not significantly change in the all tissues. The observations presented led us to conclude that the administration of subchronic TCA promotes lipid peroxidation content, elevates tissue damage serum marker enzymes and fluctuates in the antioxidative systems in rats. Also the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with the determined changes suggest that TCA produced substantial systemic organ toxicity in the erythrocyte, liver, brain and kidney during the period of a 50-day subchronic exposure.     

Influence of subacute and subchronic treatment of abcisic acid and gibberellic acid on serum marker enzymes and erythrocyte and tissue antioxidant defense systems and lipid peroxidation in rats

This study describes the subacute and subchronic effects of two plant growth regulators (PGRs) [abcisic acid (ABA) and gibberellic acid (GA₃)] on serum marker enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), γ-glutamil transpeptidase (GGT)], antioxidant defense systems [reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation level (Malondialdehyde = MDA) in various tissues of rats. Rats (Sprague-Dawley albino) were exposed to 75 ppm (parts per million) of ABA and GA₃. Seventy-five parts per million of PGRs as drinking water was administered orally ad libitum for 25 and 50 days continuously. The PGRs treatments caused different effect on the serum marker enzymes, antioxidant defense systems and the content of MDA in comparison to those of control rats. Results show that ABA caused a significant decrease in serum LDH and CPK activity with both periods. Also, GA₃ significantly decreased serum AST, CPK, and LDH activity with subacute and decreased serum ALT, CPK, LDH, and GGT treated with subchronic periods. The lipid peroxidation end product MDA significantly increased in the erythrocyte, liver, brain, and muscle of rats treated with both the period of GA₃ without significantly change in the erythrocyte and muscle of rats treated with the subacute period of ABA. The GSH levels were significantly depleted in the erythrocyte and brain of rats treated with both the period of GA₃ without any change in the erythrocyte, liver, brain, and muscle of rats treated with both the period of ABA. Also GSH levels in the muscle significantly depleted with the subchronic period of GA₃. Antioxidant enzyme activities such as SOD significantly decreased in the erythrocyte, liver and brain tissues but increased in the muscle tissue of rats treated with both the periods of GA₃. Meanwhile, SOD significantly decreased in liver and brain, and increased in muscle of rats treated with both the period of ABA. While CAT significantly decreased in the all tissues of rats treated with both the period of GA₃, decreased in the liver and muscle of rats treated with both the periods of ABA too. On the other hand, the ancillary enzyme GPx and GR activity in the erythrocytes, liver, brain and muscle were either significantly depleted or not changed with two periods of PGRs. The drug metabolizing enzyme GST activity significantly decreased in the brain of rats treated with subacute period of PGRs but increased in the erythrocytes of rats treated with subacute period of GA₃. As a conclusion, ABA and GA₃ had significantly increased the activity of hepatic damage enzymes. Also the rats resisted to oxidative stress via antioxidant mechanism. However, the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, and muscle during the period of a 25-day subacute and 50-day subchronic exposure.     

梨黑星病菌被哈茨木霉感染后抗氧化系统的变化

测定被哈茨木霉感染后梨黑星病菌抗氧化系统变化的结果表明,被哈茨木霉感染后梨黑星病菌过氧化氢酶、过氧化物酶和超氧化物歧化酶的活性逐渐下降;丙二醛含量和超氧阴离子产生速率上升;还原型谷胱甘肽和抗坏血酸含量降低。初步明确,梨黑星病菌被哈茨木霉感染后,活性氧清除系统等被破坏,膜脂过氧化作用加强,是最终导致菌体受害的原因之一。     

Effect of α tocopherol and selenium on antioxidant status, lipid peroxidation and hepatopathy induced by malathion in chicks

The objective of the present study was to investigate the role of α tocopherol and selenium on malathion induced hepatic damage, and antioxidant defense in chicks. The chicks were divided into three groups. First group received malathion 10 mg/kg BW, orally for 60 days, the second group received the same dose of malathion but was supplemented with α tocopherol and selenium for 60 days and the third group served as the control. A compromised antioxidant capacity as evidenced by increased levels of erythrocytic lipid peroxidation and decreased concentration of vitamin E and decreased activity of glutathione peroxidase was observed in chicks following the administration of malathion. An improved antioxidant status was observed in chicks of second group with α tocopherol and selenium supplementation including higher concentration of vitamin E, increased activity of glutathione peroxidase and lower levels of lipid peroxidation. Histopathological studies of liver in the chicks which received malathion exhibited, moderate to severe degenerative and necrotic changes in the hepatocytes. The correlation of decreased antioxidant status of chicks with degenerative changes in liver suggests that lipid peroxidation may be one of the important mechanism in the chronic toxicity of malathion. The results indicate that α tocopherol and selenium were effective in partially alleviating degenerative changes induced by malathion in the liver of chicks by attenuating processes leading to lipid peroxidation.     

Protective effects of caffeic acid phenethyl ester on rotenone-induced myocardial oxidative injury

Rotenone, an insecticide, causes toxicity through inhibition of mitochondrial electron transport chain at complex I and oxidative injury to the tissues. The aim of the present study was to determine in vivo effects of rotenone on myocardium and cardio-protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, against rotenone toxicity in rats. The rats were divided into three groups: untreated control, rotenone (2.5 mg/kg/day for 60 days, i.p.) and rotenone + CAPE groups. CAPE was administrated i.p. 10 μmol/kg/day for 62 days started two days before first dose rotenone injection. The malondialdehyde, nitric oxide levels and xanthine oxidase activity of rotenone group was significantly higher than control and rotenone + CAPE groups (p < 0.05). However, catalase activity in the rotenone group was decreased in comparison with the other groups (p < 0.05). The superoxide dismutase activity of rotenone group was insignificantly decreased compared to the others. In conclusion, rotenone caused lipid peroxidation in myocardial tissue and CAPE treatment prevented this rotenone-induced lipid peroxidation in rats. CAPE might be a cardio-protective agent against myocardial toxicities.     

Effects of indoleacetic acid and kinetin on lipid peroxidation and antioxidant defense in various tissues of rats

This study aims to investigate the effects of indoleacetic acid (IAA) and kinetin (Kn), which are plant growth regulators (PGRs), on antioxidant defense systems [reduced glutathione (GSH), glutathione-S-transferase (GST), catalase (CAT)], and lipid peroxidation level (malondialdehyde, MDA) various tissues of rats. Rats (Sprague-Dawley albino) were exposed to 100 ppm IAA and Kn. One hundred parts per million of PGRs was administered orally to rats ad libitum for 21 days continuously. The PGRs treatments caused different effects on the content of MDA and antioxidant defense system in comparison to those of control rats. According to the results, the subchronic treatments of IAA caused significant decrease in the GSH concentration and CAT activity in erythrocyte. Kn decreased GSH concentration in erythrocyte too. While the MDA concentration in brain was increased significantly by IAA and Kn, Kn decreased significantly brain CAT and GST activity. The liver GST activity was decreased by IAA and Kn. But, liver CAT activity was increased by IAA. On the other hand, while IAA treatment caused a significant decrease kidney GST activity, Kn caused a significant decrease both kidney GST and CAT activity. Also, while heart CAT activity was decreased by IAA, heart GST activity was decreased by both IAA and Kn. Moreover, MDA concentration in heart was increased by Kn treatment. It was concluded that IAA might effect MDA and antioxidant defense on the animals at subchronic treatment.     

Comparative studies on chlorpyrifos and methyl parathion induced oxidative stress in different parts of rat brain: Attenuation by antioxidant vitamins

Organophosphate (OP) pesticides are among the most widely used synthetic chemicals for controlling a wide variety of pests. Chlorpyrifos (o,o′-diethyl-o-3,5,6-trichloro-2-pyridyl phosphorothionate, CPF) is among the leading OP pesticides used extensively throughout the world including India while methyl parathion (o,o-di methyl-o-p-nitrophenyl phosphorothioate, MPT) another OP compound, widely used as insecticide and acaricide to control many biting or sucking pests of agricultural crops. Present study was carried out to compare the chronic toxicity of CPF and MPT, their potential to generate oxidative stress and ameliorating effects of antioxidant vitamins in brain of rats. Results of the present study clearly demonstrated that the oral exposure of CPF or MPT, generated oxidative stress in different parts of rat brain consequently accumulating malondialdehyde (MDA) and 4-hydroxynonanal (4HNE), the two major end products of lipid peroxidation, in all the three brain regions i.e. fore-, mid- and hind-brain. The levels of hydrogen peroxide (H₂O₂) were also increased in all the three brain regions when compared with control. CPF and MPT exposure caused decrease in the levels of reduced glutathione (GSH) and increase in the levels of oxidized glutathione (GSSG) in all the three brain regions. The increase in the levels of MDA, 4HNE, H₂O₂ and GSSG was less pronounced when CPF or MPT was given to the rats fed with a mixture of vitamin A, E and C. The present findings clearly show that oral intake of a mixture of vitamin A, E and C protects the rats from MPT or CPF induced oxidative stress and suggest that this treatment alleviates the toxicity of these pesticides to a greater extent.     

类黄酮在草甘膦诱导的苦荞膜脂过氧化中的作用

研究了草甘膦对苦荞类黄酮次生代谢的影响及类黄酮与草甘膦作用下膜脂过氧化伤害的关系，以探讨植物类黄酮代谢的意义及在草甘膦伤害中的作用机制。结果表明，分别用浓度为0．1、0．3、1mmoL／L的草甘膦处理苦荞幼苗，苦荞类黄酮代谢受到明显抑制，处理3天时类黄酮含量比对照分别下降58．1％、65．8％和76．5％。草甘膦处理导致苦荞膜脂过氧化加剧，0．1mmoL／L草甘膦处理使苦荞相对电导率增加275．4％、丙二醛（MDA）含量增加134．1％、超氧自由基O2^-产生速率增加121．7％，且随草甘膦浓度升高而增加幅度加大，说明草甘膦伤害与膜脂过氧化程度有关。0．3mmoL／L草甘膦处理后再用0．1mmoL／L类黄酮物质芦丁处理，电解质外渗下降34．2％，MDA含量下降51．1％，O2^-产生下降33．9％，明显减轻了草甘膦的伤害，这说明草甘膦作用下类黄酮含量的下降与草甘膦对苦荞组织伤害有一定的关系。     

Modulation of ethion-induced hepatotoxicity and oxidative stress by vitamin E supplementation in male Wistar rats

Organophosphorus insecticides (OPIs) may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system of animals. Many studies reported that enzymatic and non-enzymatic antioxidant may play protective role against OPIs induced toxicity in human and rats. The aim of present study was to investigate the possible protective role of vitamin E on ethion-induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult male albino rats of Wistar strain were randomly divided into four groups; each group consists of six animals. Animals were treated for a period of 28 days. Group I (control group received corn oil); Group II [ethion treated (2.7 mg/kg bw/day)]; Group III (vitamin E treated (50 mg/kg of bw/day)]; Group IV (ethion + vitamin E treated). Animals were sacrificed after 7, 14, 21 and 28 days by decapitation and liver tissue was used for the measurement of proteins, lipid peroxidation (LPO), reduced glutathione (GSH) content and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-S-transferase (GST). Erythrocytes were analyzed for acetyl cholinesterase activity. The result of this study shows that in vivo administration of ethion caused a significant induction of oxidative damage in liver tissue as evidenced by increased level of LPO and decreased GSH content. Ethion toxicity also led to a significant increase in the activities of SOD, CAT, GPx and GST in liver tissue. In addition, decrease in GR activity was observed in ethion administered rats compared to control. Histopathological findings revealed that exposure to ethion caused damage in liver tissue. However, simultaneous supplementation with vitamin E restored these parameters partially. In conclusion, the results of the current study revealed that ethion-induced toxicity caused lipid peroxidation, alterations in the antioxidant enzymes and histopathological changes in liver. Supplementation of vitamin E exhibited protective effect by inhibiting ethion-induced toxicity in liver and erythrocytes.     

Protective effect of vitamin C against chlorpyrifos oxidative stress in male mice

Pesticides may induce oxidative stress leading to generate free radicals and alternate antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the acute toxicity of chlorpyrifos toward male mice and the oxidative stress of the sub-lethal dose (1/10 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) activities. Also, the protective effects of vitamin C (200 mg/kg body weight, bw) 30 min before or after administration of chlorpyrifos were investigated. The results demonstrated that the LD₅₀ value of chlorpyrifos was 134.95 mg/kg bw. The oral administration of 13.495 mg/kg chlorpyrifos significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD and GST. However, GPx activity remained unchanged, while the level of GSH and G6PD activity were decreased. Vitamin C treatment to chlorpyrifos intoxicated mice decreased LPO level and GST activity, normalized CAT, SOD and G6PD activities, while GSH content was increased. We conclude that vitamin C significantly reduces chlorpyrifos-induced oxidative stress in mice liver and the protective effect of the pre-treatment with vitamin C is better than the post-treatment.     

Toxic effects of novel organophosphorus insecticide (RPR-V) on certain biochemical parameters of euryhaline fish, Oreochromis mossambicus

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (0.017 mg L⁻¹) of a novel phosphorothionate, 2-butenoic acid-3-(diethoxy phosphinothionyl) ethyl ester (RPR-V) for 30 days and allowed to recover for 7 days. Important biomarker enzymes were assayed in plasma, brain, gill, liver, kidney, and muscle during exposure tenures of day-3, -7, -15, -30, and also at 7 days (withdrawal) after stopping treatment. Acetylcholinesterase (AChE) activities of brain, gill, and muscle were strongly inhibited by 67, 75, and 66%, respectively, on day-30. Exposure (time) dependent increases in alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT), acid phosphatase (AcP), and alkaline phosphatase (AkP), activities in plasma and kidney; AcP and AkP activities in gill were noticed. However, significant decrease in ALAT, ASAT, AcP, and AkP activities in liver was observed. The depletion of glycogen was observed in liver, brain, and gill tissues, an indication of typical stress related response of the fish with pesticide. A significant increase in lactate dehydrogenase (LDH) activity in gill and brain was observed and decreased in liver and muscle, indicating tissue damage and muscular harm. Depletion of glutathione (GSH) was observed in the above tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic glutathione-S-transferase (GST) levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters, in all the tissues of fish after a recovery period of 7 days. These results revealed that RPR-V affects the intermediary metabolism of O. mossambicus and the increase of biomarker enzymes in plasma, might be due to the necrosis of liver.     

Amelioratory effect of vitamin E on organophosphorus insecticide diazinon-induced oxidative stress in mice liver

Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of organophosphate insecticides (OPIs), the aim of this study was to investigate the ameliorative properties of vitamin E (vitE) against the subchronic effect of diazinon (DZN) on oxidative damage markers such as lipid peroxidation (LPO) and the antioxidant defense system (ADS) in the liver of male MFI albino mice. The groups were intraperitoneally (i.p) administered with either vehicle or vitE (100 mg/kg body weight) or ¼ LD₅₀ of DZN (16.25 mg/kg b.w.) or ½ LD₅₀ of DZN; 32.5 mg/kg b.w) or ¼ LD₅₀-DZN + vitE or ½ LD₅₀ + vitE every consecutive day for 14 days. Hepatic damage markers analysis revealed that alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly decreased in both DZN doses. Also, the significantly increased levels of biomarkers of oxidative stress as LPO and protein carbonyl (PC) and the decreased antioxidant defenses like reduced glutathione (GSH), and free radical scavenger enzymes viz., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rx) were noted in DZN-treated groups as compared to control group. Distinctly lower levels of GSH and increased levels of LPO, along with alterations in endogenous antioxidant enzymes were evident in hepatic toxicity of DZN which is dose-dependent. Hepatic specific marker enzymes were restored to normalcy in mice supplemented with vitE following treatment with DZN which otherwise was decreased in the DZN-treated mice. The results show that co-treatment of vitE with DZN prevents or diminishes the oxidative stress of DZN-treated mice and may act as a putative protective agent against DZN-induced liver tissue injury.     

Antioxidant role of propolis extract against oxidative damage of testicular tissue induced by insecticide chlorpyrifos in rats

Pesticides induce oxidative stress leading to generate free radicals and alternate the antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the oral toxicity of chlorpyrifos toward male rat and the oxidative stress of the sub-lethal dose (9 mg/kg; 1/25 LD₅₀) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities of testicular tissue. Also, the protective effects of propolis extract (50 mg/kg b.w.) alone or in combination with chlorpyrifos were investigated. The oral administration of chlorpyrifos significantly caused elevation in LPO level by 1.79-fold as compared to control. The activities of antioxidant enzymes including CAT, SOD, GPx and GST were decreased significantly (23.66%, 27.75%, 29.13% and 11.52%) as well as the level of GSH decreased by 21.97% in testicular tissue as compared to control animals. Co-administration of propolis extract with chlorpyrifos or alone in male rats decreased LPO level, normalized CAT, SOD GPx and GST activities, while GSH content was increased in testicular tissue. We conclude that propolis extract significantly reduces chlorpyrifos-induced oxidative stress in rat testis and the protective effect of the pre-treatment with propolis extract as attenuating agent could be due to its antioxidant properties.     

夏玉米不同生育期对水分胁迫的生理反应与适应

利用大型活动遮雨棚池栽对夏玉米进行了出苗后的全程水分控制试验研究,探讨了不同生育期夏玉米叶面积、根系活力、叶片膜脂过氧化以及保护酶超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性对不同水分胁迫的生理反应与适应。结果表明:轻度受旱在大喇叭口至抽雄初期对植株叶面积影响不大,但抽雄后直至灌浆中期,轻度受旱持续时间长了也会对叶面积造成较大的不良影响。而重旱胁迫在各生育时期对叶面积的影响更为不利。干旱胁迫下,夏玉米生育进程中保护酶SOD、POD和CAT活性基本呈现一致下降的态势,膜脂过氧化作用增强,从而引发细胞内膜系统直接受损,可能是干旱逆境下作物主要的生理反应。各生育阶段因受旱时间和强度的不同,三个保护酶活性下降及膜脂过氧化产物丙二醛(MDA)积累均表现不同,随干旱胁迫的推进,短时期内对某些保护酶有一定的激发效应,即在大喇叭口期SOD和POD的活性有所增加,但此效应维持不长,其后骤降。受旱时间越长,受旱程度越重,则保护酶活性越低,MDA积累越多。根系对土壤干旱胁迫甚为敏感,玉米拔节期根系活力下降就见端倪,随受旱的延长及加剧将更加促使根系老化,根系活力快速衰减。