2,4-D and MCPA and their derivatives: Effect on the activity of membrane erythrocytes acetylcholinesterase (in vitro)

The effect of 2,4-dichlorophenoxyacetic acid (2,4-D), 4-chloro-2-methylphenoxyacetic acid (MCPA), and their derivatives: phenol, 2,4-dichlorophenol (2,4-DCP), 2,4-dimethylphenol (2,4-DMP), and catechol on the activity of acetylcholinesterase (AChE, EC 3.1.1.7) in human erythrocytes was studied. Phenol, MCPA, and 2,4-DMP did not significantly change AChE activity in human erythrocytes (in vitro). Decrease of AChE activity was observed under the highest applied dose of 2,4-D—500 and 1000 ppm. Decrease of AChE activity exposed to 2,4-DCP and catechol was noted and depended on the doses of applied compounds. The relationship between activities and substrate concentrations (curves) was analyzed for reactions of acetylcholinesterase. Catalytic constants K_m and V_max were calculated from the Michaelis curve. Statistically significant decrease of V_max and K_m was observed in the activity of AChE incubated with 2,4-DCP and catechol, revealing mixed inhibition type of AChE inhibition (this compound may affect not only on enzyme but also on complex ES as well). 2,4-D decreases V_max but do not change K_m value, what reveals non-competitive type of AChE inhibition by this compounds. Non-competitive inhibition does not depend on the substrate concentrations but only on the inhibitor concentration and its K_i value, characterizes the affinity of inhibitors towards enzyme. In conclusion, changes of AChE activity upon 2,4-D, 2,4-DCP, and catechol are the consequences of direct interactions between compounds and the enzyme and indirect via membrane modification and increase of Reactive Oxygen Species.     

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.     

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.     

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.     

Allelochemical ethyl 2-methyl acetoacetate (EMA) induces oxidative damage and antioxidant responses in Phaeodactylum tricornutum

Ethyl 2-methyl acetoacetate (EMA) is a novel allelochemical exhibiting inhibitory effects on the growth of marine unicellular alga Phaeodactylum tricornutum (P. tricornutum). Oxidative damage and antioxidant responses in P. tricornutum were investigated to elucidate the mechanism involved in EMA inhibition on algal growth. The increase in reactive oxygen species (ROS) levels and malondialdehyde (MDA) contents following exposure to EMA suggested that alga was suffered from oxidative stress and severely damaged. The decrease in cell activity and cellular inclusions suggested that cell growth was greatly inhibited. The activities of the antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxide (GSH-PX) and glutathione S-transferase (GST) increased with the exposure concentration and decreased with the prolongation of exposure time. Cellular ascorbic acid (AsA) and reduced glutathione (GSH) systems were also involved in resisting oxidative stress of EMA by altering the composition of AsA and GSH pools. EMA exposure increased the contents of AsA, GSH, dehydroascorbate (DAsA) and glutathione (GSSG). However, the regeneration rate of AsA/DAsA did not change obviously between treatments and the control, while that of GSH/GSSG decreased significantly under 14 mmol/L EMA exposure on the 3rd day. These results showed that EMA-induced oxidative damage might be responsible for EMA inhibition on P. tricornutum growth and cellular antioxidant enzymes and non-enzymatic antioxidants were improved to counteract the oxidative stress.     

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.     

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.     

Oxidative damage in bone and erythrocytes of suckling rats exposed to 2,4-dichlorophenoxyacetic acid

Nowadays, people’s exposure to pesticides such as 2,4-dichlorophenoxyacetic acid (2,4-D) is increasing continuously. This compound is suspected to produce in excess free radicals which have adverse effects on human health causing several cell alterations in the organism. The present study investigated oxidative stress in the bone and erythrocytes of suckling rats whose mothers were treated with 2,4-D. Experiments were carried out on adult Wistar rats given 600 mg/L of 2,4-D in their drinking water from the 14th day of pregnancy until day 14 after delivery. Exposing dams to 2,4-D caused disorders in the bone of their progeny. Indeed, it induced changes in bone mineralization, especially calcium and phosphorus levels. Moreover, total tartrate-resistant acid phosphatase, which reflected bone resorption, was enhanced while total alkaline phosphatase, which reflected bone formation, was reduced suggesting that this herbicide accelerated bone resorption. The impairment of bone function corresponded histologically.Rats exposed to 2,4-D showed in both bone and erythrocytes an increase in malondialdehyde, advanced oxidation protein products and protein carbonyl levels and a decrease in non-enzymatic (glutathione, non-protein thiol, and vitamin C) and enzymatic (superoxide dismutase, catalase, and glutathione peroxidase) antioxidant system.     

Acute effects of methyl parathion and diazinon as inducers for oxidative stress on certain biomarkers in various tissues of rainbowtrout (Oncorhynchus mykiss)

Present study aimed mainly to assess oxidative stress pesticides such as methyl parathion (MP) and diazinon, which are widely used insecticides and contaminate aquatic ecosystems, on certain biomarkers in various tissues of rainbowtrout (Oncorhynchcus mykiss). Biomarkers selected for stress monitoring were malondialdehyde (MDA) and antioxidant defense system (ADS) mainly reduced glutathione (GSH), glutathione reductase (GR), peroxidase (GSH-PX), transferase (GST) and superoxidedismutase (SOD) activities in the liver, gills and muscle of fishes exposed to 0.5 and 1 ppm dosages of MP and diazinon for 24, 48 and 72 h. According to these results, after the administrations of MP and diazinon promote MDA content in some of the tissues of fishes treated with both dosages of MP and diazinon. With regard to the ADS, GSH-Px, GST, SOD, GR activities and GSH levels fluctuated after 24, 48 and 72 h in all the treatment groups compared with controls. Collective results demonstrated that exposure of fish to pesticides induced an increase in MDA joined with fluctuated ADS. This may reflect the potential role of these parameters as useful biomarkers for assessment of water pollution.     

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.     

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.     

Protective effects of Nigella sativa oil on propoxur-induced toxicity and oxidative stress in rat brain regions

Propoxur (PPr) is a widely used broad spectrum carbamate insecticide mainly used to control household pests. Because of the widespread use of pesticides for domestic and industrial applications, evaluation of their neurotoxic effects is of major concern to public health. The aim of the present study was to evaluate the possible protective effects of Nigella sativa oil (NSO), an antioxidant agent, against PPr-induced toxicity and oxidative stress in different brain regions of rats including cerebellum, cortex and hippocampus. In the present study, 32 male Sprague-Dawley rats were used and divided into four equal groups. Group 1 was allocated as the control group. Groups 2-4 were orally administered 1 ml/kg/bw/day NSO, 8.51 mg/kg/bw/day PPr or NSO plus PPr, respectively, for 30 days. Lipid peroxidation (LPO), protein carbonyl content (PCC) and acetylcholine esterase activity (AChE) were determined. Enzymatic antioxidant activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST)] and non-enzymatic antioxidants [reduced glutathione (GSH)] were determined. PPr treatment significantly increased the levels of LPO, PCC and oxidized glutathione (GSSG) in brain regions. On the contrary, levels of GSH and the activities of SOD, CAT, GSH-Px, GST and AChE were significantly decreased. NSO treatment to PPr intoxicated rats restored such biochemical parameters to within control levels except GST activity, emphasizing its antioxidant role. We conclude that NSO significantly reduces PPr-induced toxicity and oxidative stress in rat brain regions via a free radicals scavenging mechanism.     

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 effect of reduced glutathione on the respiratory muscle injury induced by acute omethoate poisoning

The aim of this work was to investigate whether reduced glutathione (GSH) could protect rats from the respiratory muscle injury induced by omethoate. Three groups named as control, OM (omethoate poisoning) and OM + GSH (omethoate poisoning treated with GSH) were arranged. The cholinesterase (ChE) activity was assayed and the pathological observation of respiratory muscles was carried out. Furthermore, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and the free organophosphate (FOP) remained in the respiratory muscles were measured. The results indicated that ChE activity was significantly inhibited by omethoate and not be changed by GSH. GSH could attenuate the respiratory muscle injury after omethoate poisoning. No changes of SOD, GPx, CAT and FOP were found after GSH was given. The findings suggested that GSH could protect the respiratory muscle against injury induced by omethoate, which was not the result of GSH to reactivate ChE or regulate the antioxidant enzymes.     

Protective effect of reduced glutathione on the respiratory muscle injury induced by acute omethoate poisoning

The aim of this work was to investigate whether reduced glutathione (GSH) could protect rats from the respiratory muscle injury induced by omethoate. Three groups named as control, OM (omethoate poisoning) and OM + GSH (omethoate poisoning treated with GSH) were arranged. The cholinesterase (ChE) activity was assayed and the pathological observation of respiratory muscles was carried out. Furthermore, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and the free organophosphate (FOP) remained in the respiratory muscles were measured. The results indicated that ChE activity was significantly inhibited by omethoate and not be changed by GSH. GSH could attenuate the respiratory muscle injury after omethoate poisoning. No changes of SOD, GPx, CAT and FOP were found after GSH was given. The findings suggested that GSH could protect the respiratory muscle against injury induced by omethoate, which was not the result of GSH to reactivate ChE or regulate the antioxidant enzymes.     

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.     

天然芸苔素内酯缓解胺苯磺隆对后茬水稻药害的作用机理初探

通过测定天然芸苔素内酯对水稻幼苗谷胱甘肽(GSH)含量、谷胱甘肽-S-转移酶(GST)活性以及在离体和活体条件下对水稻幼苗乙酰乳酸合成酶(ALS)活力的影响,研究天然芸苔素内酯减轻胺苯磺隆对水稻药害的作用机理。结果表明,其作用机理与水稻幼苗GSH含量、GST活性变化没有太大相关性,可能与其能间接激活水稻幼苗ALS活力有较大相关。     

Coexpression with Auxiliary β Subunits Modulates the Action of Tefluthrin on Rat Na(v)1.6 and Na(v)1.3 Sodium Channels

The erythrocyte, due to its role as O₂ and CO₂ transporter, is under the constant exposure to reactive oxygen species and oxidative stress. The objective of this study was to investigate the ability of 2,4-D to induce oxidative stress in blood of male wistar rats. Rats were randomly divided into four groups: a control group and three treated groups receiving by gavage 15, 75 and 150 mg, respectively, of 2,4-D/kg/BW/day for 28 days. Results showed that 2,4-D caused significant negative changes in the investigated biochemical parameters. In fact, 2,4-D exposition strongly increases LDH, by contrast, there is a statistically significant decrease in Hgb levels. The malondialdehyde level was significantly increased in 2,4-D treated groups. Fatty acid composition of the erythrocytes was also significantly changed with 2,4-D exposure, in favor of the peroxidation of polyunsaturated fatty acids. Furthermore, antioxidant enzyme (SOD, CAT, GPx, and GR) activities in erythrocytes were significantly decreased. Thus, our results indicated the potential effects of 2,4-D to cause oxidative stress in rat erythrocytes. Therefore, at higher doses, 2,4-D may play an important role in the development of vascular disease via lipid peroxidation and oxidative stress.     

Dimethoate induced biochemical perturbations in rat pancreas and its attenuation by cashew nut skin extract

The significant antiradical activity of cashew skin extract was previously described. In this investigation, the extent of protection offered by cashew nut skin extract (CSE) against the damage induced in rat pancreas by sub chronic doses dimethoate (DM), an organophosphorous pesticide was studied. Rats were supplemented with CSE at 20 mg/kg b.w./d after a daily dose of DM at 40 mg/kg/d b.w. for 2 months. Weekly random blood glucose, oral glucose tolerance test (OGTT); pancreatic damage markers like amylase and lipase; oxidative damage markers such as reactive oxygen species generated, extent of lipid peroxidation, host antioxidant defenses like reduced glutathione (GSH); GSH-dependent enzyme activities viz., glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR); free radical scavenger enzymes viz., catalase and superoxide dismutase (SOD); xenobiotic metabolizing enzymes like DT-diaphorase and NADPH-diaphorase were measured in the four different groups namely (1) control, (2) DM treated, (3) CSE supplemented, (4) CSE supplements following DM treatment. Random blood glucose levels increased significantly on exposure to DM compared to that in control rats (119 ± 5 mg/dl vs. 92 ± 4 mg/dl), while the blood glucose levels in CSE supplemented rats were comparable to that of controls. DM treated rats exhibited impaired glucose tolerance at the end of two months as indicated by OGTT, while DM treated rats with CSE supplements showed normal glucose tolerance. Pancreatic specific marker enzymes like amylase and lipase in serum were restored to normalcy in rats supplemented with CSE following treatment with DM which otherwise was increased in the DM treated rats. Distinctly lower levels of GSH, increased levels of ROS, higher extent of lipid peroxidation, along with alterations in antioxidant enzymes and increase in xenobiotic metabolizing enzymes were evident in pancreas of DM treated rats. However, CSE supplement ameliorated the biochemical alterations in the pancreatic milieu in DM treated rats. Treatment with CSE significantly protected rat pancreas from injury, thus ameliorating and restoring tissue antioxidant status and also conferring normal glucose tolerance. The active components present in cashew skin extract can perhaps be effective in reducing the extent of pancreatic injury and in overcoming tissue damage caused by exposure to dimethoate.