Influence of three diets on susceptibility of selected insecticides and activities of detoxification esterases of Helicoverpa assulta (Lepidoptera: Noctuidae)

The oriental tobacco worm, Helicoverpa assulta Guenée, is one of the most destructive pests of tobacco and peppers in China. We determined the susceptibility of H. assulta reared on an artificial diet, chili pepper and tobacco to four insecticides (fenvalerate, phoxim, methomyl, indoxacarb) under laboratory conditions associated with the activities of acetylcholinesterase (AChE), carboxylesterase (CarE) and glutathione S-transferase (GST) in its larvae. H. assulta larvae that were fed with chili pepper were more susceptible to fenvalerate, indoxacarb, and phoxim than those that were fed with tobacco and the artificial diet, but not to methomyl. The larvae that were fed with chili pepper were 3.65-, 2.49-, 1.92- and 2.44-fold more susceptible to fenvalerate, phoxim, methomyl, and indoxacarb than those fed with tobacco, respectively. The AChE activities of H. assulta larvae that were fed with chili pepper and tobacco were 2.12 and 1.07 μmol mg⁻¹ 15 min⁻¹, respectively, almost 2-fold difference. The CarE activity of H. assulta larvae that were fed with chili pepper, tobacco and the artificial diet was 4.12, 7.40 and 7.12 μmol mg⁻¹ 30 min⁻¹, respectively. Similarly, the GST activities of H. assulta larvae that were fed with chili pepper, tobacco and the artificial diet was 52.02, 79.37 and 80.02 μmol mg⁻¹ min⁻¹, respectively. H. assulta larvae that were fed with chili pepper were more resistance to the tested insecticides. The low activities of AChE and the high activities of CarE and GST lead to H. assulta become more susceptible to the tested insecticides.     

Tissue-specific antioxidative and neurotoxic responses to diazinon in Oreochromis niloticus

The purpose of this study was to evaluate oxidative stress and neurotoxic potential of organophosphorus (OP) insecticide diazinon in the sentinel freshwater fish, Oreochromis niloticus. Antioxidant and acetylcholinesterase (AChE) enzyme activities and malondialdehyde (MDA) and protein levels were measured spectrophotometrically in gill, kidney, alimentary tract, and muscle tissues of fish treated with sub-lethal diazinon concentrations for 1, 7, 15, and 30 days. Dose-dependent inhibitions of AChE were observed in all the experimental fish. On the contrary of alimentary tract, MDA levels were elevated in kidney and muscle and gill was not affected. AChE and MDA levels intercorrelated in kidney and muscle tissues. Diazinon had increased superoxide dismutase (SOD) activities in all the tissues, while kidney was the most affected tissue. Tissue-specific alterations were observed on catalase (CAT) and glutathione peroxidase (GPx) activities; however, the activities were not changed in gill and muscle tissues for GPx and in gill, muscle, and kidney tissues for CAT. Protein levels decreased in kidney, muscle, and alimentary tract, while increased in gill and alimentary tract in 15 days. With respect to these results, diazinon has oxidative and neurotoxic potentials in O. niloticus. Observed changes with diazinon treatment were generally tissue-specific and dose-dependent.     

Exposure to streptomycin alters oxidative and antioxidative response in larval midgut tissues of Galleria mellonella

Although antibiotics have different molecular modes of actions, increasing evidence for their secondary effects suggests that they disturb cellular homeostasis by generating free radical intermediates that trigger lipid peroxidation, which leads to oxidative stress. Streptomycin is an antibiotic insecticide used to control pest insects and microbial diseases of agricultural crops. We investigated the biochemical basis for pro-oxidative effects of streptomycin in the midgut tissues of greater wax moth, Galleria mellonella (L.) seventh-instar larvae by measuring content of the oxidative stress indicator, malondialdehyde (MDA), and antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GPx)] and transaminases [alanine aminotransferase (ALT), aspartate aminotransferase (AST)] activities. The insects were reared from first-instar larvae on artificial diets containing 0.001, 0.01, 0.1 or 1.0 g streptomycin per 100 g of diets. The supplementation of streptomycin at high concentrations to the diets caused oxidative stress as evidenced by the elevation of MDA content, SOD and GPx activities, accompanied by the concurrent depletion of CAT and GST activities. The streptomycin-induced oxidative stress was also accompanied by decreases of transaminases activities in midgut tissues. We found a significant negative correlation of MDA contents with GST activities in the larval midgut tissues. These results suggest that exposure to dietary streptomycin resulted in oxidative stress which could impact midgut digestive physiology at the expense of impairment of antioxidant and transaminases enzymes in G. mellonella larvae.     

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.     

Biochemical and histological hepatic changes of Nile tilapia Oreochromis niloticus exposed to carbaryl

The purpose of this study was to evaluate biochemical and morphological responses induced by carbaryl in the liver of Nile tilapia (Oreochromis niloticus) exposed during 21 days to sublethal concentrations (0.25 and 0.5 mg L⁻¹), testing also recover for 14 days in clean water, after 14 days exposure. The activities of the following enzymes were measured: superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR), and reduced (GSH) and oxidized glutathione (GSSG). Globally, our data showed that exposure to carbaryl decreased the SOD, CAT, GR, and GST activities, except for the SOD and GST activities after 14 days exposure to 0.25 mg L⁻¹. In contrast, after 14 days exposure the GR activity of the hepatic tissue from carbaryl-treated fish showed significant elevation in relation to the control. When fish were left to recover, a positive response was seen in the GSH and GSSG contents. The results of the recovery group suggest that the toxicity produced by carbaryl is reversible to some extent within 15 days. The liver histological analysis showed differences between fish concerning the cellular vacuolization degree (VD) of the hepatocytes. In fish exposed to carbaryl it was observed an increasing hepatocellular basophilia. No other histological alterations were observed when fish was exposed to carbaryl, except a few necrotic foci at day 7. The sections stained with PAS reaction showed that the vacuolization was always not due to glycogen deposits, thus suggesting lipid accumulation. The combined increased basophilia and glycogen depletion is a common, although non-specific, liver response to many toxicants. In short, this work shows a relation between histological and biochemical changes in liver and carbaryl exposure. The effects of carbaryl were observed at different concentrations.     

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.     

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.     

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.     

Evaluation of etoxazole toxicity in the liver of Oreochromis niloticus

The effects of etoxazole were evaluated in freshwater fish Oreochromis niloticus from five different sublethal etoxazole concentrations in order to study the biochemical response, photometrically. No changes were observed in the activities of antioxidant enzymes such as superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), and glutathione peroxidase (GPx, EC 1.11.1.9). These were measured in liver after 1, 7, and 15 days of exposure to sublethal concentrations of 0.2, 0.4, 0.6, 0.8, and 1% of field application rate (134.75 ppm). This study also investigated the levels of neurotoxic effects by the determination of acetylcholine esterase (AChE EC 3.1.1.7) and sodium-potassium adenosine 5^′-triphosphatase (Na⁺K⁺-ATPase, EC 3.6.3.9) activities. The exposure of fish led to sharp depletion in AChE activity while there is no significant alteration in Na⁺K⁺-ATPase activity. Up to 80% decreases were observed in the AChE activity. Since no difference was found in the activity of glutamate-pyruvate transaminase (GPT, EC 2.6.1.2), etoxazole did not show hepatotoxic effect. The results of the present study show that increase in the malondialdehyde (MDA) contents and decrease in the AChE activity can be used as biomarkers for monitoring toxicity in etoxazole exposure.     

Subacute chlorpyrifos-induced oxidative stress in rat erythrocytes and the protective effects of catechin and quercetin

This study examined the effects of chlorpyrifos in the rat erythrocyte antioxidant system and evaluated the ameliorating effects of catechin and quercetin on the oxidative damage induced by chlorpyrifos. Sexually mature male Wistar rats were given chlorpyrifos (5.4 mg/kg, 1/25 of the oral LD₅₀), catechin (20 mg/kg), quercetin (20 mg/kg), catechin plus chlorpyrifos, and quercetin plus chlorpyrifos daily via gavage for four weeks. No statistical differences were found in the catechin-only and quercetin-only groups compared with the control group. By the end of the fourth week, chlorpyrifos alone increased the levels of malondialdehyde (MDA) and decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities compared with the control group in rat erythrocytes. In the catechin-plus-chlorpyrifos and quercetin-plus-chlorpyrifos groups, there were statistically significantly decreased MDA levels and increased SOD, CAT, and GPx activities compared with the chlorpyrifos-only group. Thus, it appears that catechin and quercetin ameliorate chlorpyrifos-induced oxidative stress in rat erythrocytes in vivo.     

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.     

The effect of silicon on antioxidant metabolism of wheat leaves infected by Pyricularia oryzae

This study investigated whether the increase in wheat resistance to blast, caused by Pyricularia oryzae, potentiated by silicon (Si) is linked to changes in the activity of antioxidative enzymes. Wheat plants (cv. BR 18) were grown in hydroponic culture with either 0 (–Si) or 2 mm (+Si) Si and half of the plants in each group were inoculated with P. oryzae. Blast severity in the +Si plants was 70% lower compared to the ?Si plants at 96 h after inoculation (hai). Superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), ascorbate peroxidase (APX) and glutathione‐S‐transferase (GST) activities were higher in the leaves of the ?Si plants compared with the +Si plants at 96 hai. This indicates that other mechanisms may have limited P. oryzae infection in the +Si plants restricting the generation of reactive oxygen species, obviating the need for increased antioxidative enzyme activity. In contrast, glutathione reductase (GR) activity at 96 hai was higher in the +Si plants than in the ?Si plants. Although the inoculated plants showed significantly higher concentration of malondialdehyde (MDA) than the non‐inoculated plants, lower MDA concentrations were observed in the +Si plants compared with the ?Si plants. The lower MDA concentration associated with decreased activities of SOD, CAT, POX, APX and GST, suggest that the amount of reactive oxygen species was lower in the +Si plants. However, GR appears to play a pivotal role in limiting oxidative stress caused by P. oryzae infection in +Si plants.     

Oxidative stress, steroid hormone concentrations and acetylcholinesterase activity in Oreochromis niloticus exposed to chlorpyrifos

We investigated the endocrine disrupting effects of chlorpyrifos-ethyl which is suspected to be originated from oxidative stress. Initially, the 96 h LC₅₀ values of chlorpyrifos in juvenile and adult of Oreochromis niloticus were determined to be 98.67 μg/L and 154.01 μg/L, respectively. Sub-lethal concentrations of chlorpyrifos-ethyl (5 ppb, 10 ppb, 15 ppb) were administrated to adult fish for 15 and 30 days. Fish were then left to depurate for 15 days in pesticide-free water. Gonadal somatic indices, serum sex steroids as indicators of reproductive function and cortisol level as indicator of stress condition were measured to observe the endocrine disruption effects of chlorpyrifos-ethyl. Gonadal glutathione S-transferase and antioxidant enzyme activities and lipid peroxidation as indicators of oxidative stress were also measured. Acetylcholinesterase activity was measured as a marker of chlorpyrifos toxicity. Results showed that serum estradiol, testosteron and cortisol levels in fish exposed to chlorpyrifos were lower than those of the control fish while gonad somatic indices did not change during the experiments. After 30 days, chlorpyrifos exposure decreased GST activity, and increased SOD enzyme activity by up to 215-446% compared with the control, suggesting there was a oxidative stress. No statistically significant differences between GPx and CAT specific activities, protein contents and lipid peroxidation were determined between control and treatment groups in all exposure concentrations and periods. Acetylcholinesterase activity decreased (45.83-77.28%) in gonad tissues. After recovery serum estradiol and testosteron levels were similar to those of the control levels. An increase in the GST and SOD enzyme activities were determined. Cortisol level and AChE activity in all exposure groups decreased after the depuration period, and fish were unable to overcome the stress of chlorpyrifos. Thus, this study revealed that after chlorpyrifos treatments there exists a protective function of antioxidant enzymes against lipid peroxidation in gonad tissue of O. niloticus. There also exist lower testosteron and estradiol levels in exposed fish than those of the control fish without any alterations in oxidative stress, which is attributed to the capability of chlorpyrifos to impair steroid hormone levels.     

Effects of trichlorfon and sodium dodecyl sulphate on antioxidant defense system and acetylcholinesterase of Tilapia nilotica in vitro

The effects of organophosphorus insecticide trichlorfon, surfactant sodium dodecyl sulphate (SDS), and the mixture of trichlorfon and SDS on the antioxidant defense system and acetylcholinesterase (AChE) in Tilapia nilotica were assessed in vitro. Various concentrations of trichlorfon (0, 0.0001, 0.001, 0.01, 0.1 and 1 g/L) and SDS (0, 0.0625, 0.125, 0.25, 0.5, 1 g/L) were incubated with homogenate of liver and muscle, respectively, at 25 °C for 0, 30, 60 and 90 min. Two concentrations of mixture of trichlorfon and SDS (0.0001 g/L trichlorfon + 0.5 g/L SDS, 0.1 g/L trichlorfon + 0.5 g/L SDS) and 0.0001 g/L trichlorfon, 0.1 g/L trichlorfon, 0.5 g/L SDS and control, were incubated simultaneously with homogenate of liver and muscle, respectively, at 25 °C for 60 min. After incubation, the content of reduced-glutathione (GSH) and the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) in homogenate of liver were determined, and the activities of AChE in homogenate of muscle were also measured.Treatment with trichlorfon caused a significant concentration-dependent and time-related inhibition of AChE activity at all treatment concentrations and times since trichlorfon is a cholinesterase inhibitor. For the same trichlorfon treatment, an apparent decrease in GSH content was found in concentration of 0.01, 0.1, 1 g/L, whereas no significant alteration in antioxidant enzyme activity were found at all experiment concentrations and times, which might indicate that antioxidant enzymes have not involved in the metabolism of trichlorfon. The depletion of GSH might indicate that ROS could be involved in the toxic effects of trichlorfon. Exposure of SDS can inhibit activities of AChE, GST and CAT at concentrations of 0.5 and/or 1 g/L, which could be due to the denaturing process of SDS to the enzymes. For the mixture exposure of trichlorfon and SDS, the effect of the mixture of 0.0001 g/L trichlorfon and 0.5 g/L SDS on inhibition of AChE shows synergistic other than simple additive of trichlorfon and SDS. The combined effects of chemicals and detergents deserve to be particularly noted. It should be noted that the toxicity experiments were made in tissue homogenates instead of whole organisms. The responses against the toxic compounds will not be the same in both systems.     

Assessment of insecticide resistance in eggs and neonate larvae of Cydia pomonella (Lepidoptera: Tortricidae)

Spanish Cydia pomonella (L.) field populations have developed resistance to several insecticide groups. Diagnostic concentrations were established as the LC₉₀ calculated on a susceptible strain (S_Spain) for five and seven insecticides and tested on eggs and neonate larvae field populations, respectively. The three most relevant enzymatic detoxification systems (mixed-function oxidases (MFO), glutathione S-tranferases (GST) and esterases (EST)) were studied for neonate larvae.In eggs, 96% of the field populations showed a significantly lower efficacy when compared with the susceptible strain (S_Spain) and the most effective insecticides were fenoxycarb and thiacloprid. In neonate larvae, a significant loss of susceptibility to the insecticides was detected. Flufenoxuron, azinphos-methyl and phosmet showed the lowest efficacy, while lambda-cyhalothrin, alpha-cypermethrin and chlorpyrifos-ethyl showed the highest. Biochemical assays showed that the most important enzymatic system involved in insecticide detoxification was MFO, with highest enzymatic activity ratios (5.1-16.6 for neonates from nine field populations). An enhanced GST and EST activities was detected in one field population, with enzymatic activity ratios of threefold and fivefold for GST and EST, respectively, when compared with the susceptible strain. The insecticide bioassays showed that the LC₉₀ used were effective as diagnostic concentrations. Measures of MFO activity alongside bioassays with insecticide diagnostic concentrations could be used as tools for monitoring insecticide resistance in neonate larvae of C. pomonella.     

牡丹皮、黄连、大黄提取物对松材线虫生理代谢的影响

对3种中草药黄连、牡丹皮、大黄的乙醇提取物毒杀松材线虫作用机制进行了初步研究。测定了其对线虫体内总糖和蛋白含量的影响, 处理前后线虫体内超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、过氧化物酶（POD）、谷胱甘肽过氧化物酶（GSH-Px）和乙酰胆碱酯酶（AChE）酶活性变化和丙二醛（MDA）含量变化, 处理前后SOD、CAT、GSH-Px和AChE表达量变化; 并用松枝水培试验测定3种提取物对松材线虫病害的防控效果。结果表明, 提取物处理后线虫体内总糖及蛋白含量显著下降, 线虫体内糖及蛋白质的代谢受到干扰; 线虫体内SOD、CAT、GSH-Px酶活性提高, POD活性显著下降, MDA含量升高, 表明线虫体内氧化与抗氧化作用失衡, 细胞功能受到极大影响; AChE活性被抑制, 表明线虫的神经系统受到破坏, SOD、CAT、GSH-Px和POD表达量与酶活性变化基本一致。松枝水培试验表明中药提取物能够有效控制松材线虫病害发生。综上, 3种提取物引起的松材线虫体内众多生理指标的改变是造成线虫死亡的主要原因。     

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.     

二氧化碳浓度和温度升高对烟粉虱主要保护酶和解毒酶活性的影响

为明确烟粉虱Bemisia tabaci(Gennadius)在大气CO2浓度和温度双因子胁迫下的生理响应,以CO2浓度和温度为作用因子,研究了4种不同组合处理下烟粉虱成虫体内超氧化物歧化酶(SOD)、过氧化物酶(POD)、过氧化氢酶(CAT)、谷胱甘肽转移酶(GST)、乙酰胆碱酯酶(Ach E)活性的变化。结果表明:常温处理下,CO2浓度升高烟粉虱体内POD和GST活性分别增加87.6%和295%,SOD和CAT活性分别降低22.4%和28.2%;高温处理下,CO2浓度升高烟粉虱体内Ach E和GST活性分别增加103.6%和167.5%,CAT活性降低31.6%;常CO2浓度处理下,温度升高烟粉虱体内POD和SOD活性分别增加46.2%和18.2%,CAT活性降低35.8%;高CO2浓度处理下,温度升高烟粉虱体内Ach E和SOD活性分别增加75.3%和40.3%,CAT活性降低38.9%。表明CO2浓度和温度升高是导致烟粉虱体内SOD、POD、GST和Ach E活性升高的主要原因,并且SOD和POD活性变化受到CO2和温度的交互影响。烟粉虱可能通过改变体内保护酶或解毒酶的活性来适应CO2浓度和温度升高的环境。     

Oxidative stress and locomotor behaviour response as biomarkers for assessing recovery status of mosquito fish, Gambusia affinis after lethal effect of an organophosphate pesticide, monocrotophos

Recovery study was performed at regular intervals to establish the time course of 50% and 100% recovery in neurotransmitter enzyme (acetylcholinesterase, AChE, EC 3.1.1.7) and locomotor behaviour response of mosquito fish, Gambusia affinis exposed to lethal concentration (20.49 mg L⁻¹) of an organophosphorous pesticide, monocrotophos (MCP) for 96 h. In vitro AChE activity studies indicated that MCP could cause 50% inhibition (I₅₀) at 10.2 × 10⁻⁵ M. A positive correlation was observed between brain AChE activity and swimming speed during the recovery study. Also, the recovery response of the antioxidant enzymes superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6) and glutathione reductase (GR, EC 1.6.4.2) as well as lipid peroxidation (LPO) as biomarkers of oxidative stress were assessed in viscera of G. affinis. The results showed that the MCP besides its inhibitory effect on target enzyme AChE activity and induction in antioxidant enzyme activities as a characteristic of oxidative stress, which can be used as biomarkers in the pesticide contaminated aquatic streams.