五氯酚对鲫鱼肝脏的氧化损伤

将鲫鱼暴露于浓度分别为 0 .0 0 16、0 .0 16、0 .16mg·L-1的PCP溶液 15d ,同时做空白对照 ,测定鲫鱼肝脏的SOD、GSH、MDA以及NO、NOS等指标。试验结果表明 ,0 .16mg·L-1组处理的鲫鱼第 13天全部死亡。与对照相比 ,在 0 .0 0 16mg·L-1浓度下 ,PCP提高了鲫鱼肝脏MDA和NO含量 ,GSH含量降低 ,SOD活性被抑制 ,NOS活性有所升高。在 0 .0 16mg·L-1浓度组 ,PCP对几个指标的影响比 0 0 0 16mg·L-1组大 ,与对照相比 ,具有显著差异 ,说明PCP暴露可导致鲫鱼肝脏的氧化损伤     

Organophosphorous compounds and oxidative stress: a review

Organophosphorous compounds (OP) have largely been used as pesticides globally. These chemicals induce oxidative stress as a possible mechanism of action, which has been a focus of toxicological research for the last decade. This review evaluated the presence of oxidative stress, balance between total antioxidant capacity, and oxygen free radicals associated with OP compound exposure. Oxidative stress induced by OP leads to disturbances in function of different organs and tissues. Evidence indicates that stimulation of free radical production, induction of lipid peroxidation, and disturbance of the total antioxidant capacity are mechanisms of toxicity induced by most OP. Thus, use of antioxidants may be beneficial in treatment of OP poisoning, which remains to be elucidated with further clinical trials.     

Structural and molecular alterations in arsenic-induced hepatic oxidative stress in rats: a FTIR study

Arsenic (As) is an ubiquitously distributed environmental toxicant predominantly contaminating drinking water. A number of studies indicated that oral exposure of humans to inorganic As produced damage to various body tissues including liver. Oxidative stress is thought to play a major role in As-induced hepatotoxicity. In this study, Fourier transforms infrared (FTIR) spectroscopy approach was applied to determine whether chronic As exposure at 25 ppm, intragastrically for 12 weeks, affected oxidative stress status in rat liver. Data demonstrated that chronic As administration exacerbated oxidative stress as was evidenced by suppressed antioxidant defense system and increased lipid peroxidation and protein oxidation. The FTIR study showed that peak area value of amide A decreased significantly followed by reduced amide I and amide II peak area in an As-treated rat liver suggesting altered protein profile. The change of Olefinic?CH stretching band and C?O stretching of triglycerides band indicated the altered lipid levels due to metallic exposure. The fall in the peak area of PO₂^? asymmetric stretching in the As-treated group might be due to compositional changes of nucleic acids. Hence, the results of this study indicate that As-induced oxidative stress was associated with structural and molecular modifications in proteins, lipids, and glycogen in a rat liver that may help to elucidate molecular mechanisms underlying metal-mediated hepatic damage.     

Effect of repeated oral administration of bifenthrin antioxidant status and acetylcholinesterase activity in brain of rats

The oxidative-stress-inducing potential of the pyrethroid, bifenthrin, in the brain of rats was evaluated following daily oral administration of 5.8 mg/kg body weight. Lipid peroxidation in the brain was increased, while the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase decreased. The activity of acetylcholinesterase (AChE) in erythrocytes and brain also decreased. Bifenthrin induces severe oxidative stress in brain, and inhibits brain and erythrocyte AChE.     

Antioxidant role of ascorbic acid on oxidative stress induced by sub-acute exposure of lead and cypermethrin in erythrocytes of Wistar rats

This study aimed to evaluate the reparative potential of ascorbic acid (AA, 100 mg/kg, orally for 28 days) in sub-acute lead (Pb, 100 ppm in drinking water for 28 days) or cypermethrin (CPM, 50 mg/kg, orally in vehicle for 28 days) poisoning alone and as binary mixture on the basis of oxidative stress parameters in erythrocytes of Wistar rats. Both Pb and CPM produced significant increase in lipid peroxidation along with elevated glutathione-S-transferase and catalase activity individually but not as a binary mixture. Glutathione peroxidase activity was significantly increased but glutathione levels were significantly reduced irrespective of single or co-exposure while the activity of superoxide dismutase and erythrocytic protein content were not significantly affected. Co-exposure led to a comparatively lower level of oxidative stress than that induced by Pb or CPM alone indicating an antagonistic toxicodynamic profile in rat erythrocytes. Co-administration of AA along with Pb and/or CPM significantly restored the oxidative stress parameters to normal values. Overall results indicated that co-exposure induces a lower level of oxidative stress and AA ameliorates Pb- and/or CPM-induced oxidative damage in rat erythrocytes.     

Alteration of body total antioxidant capacity and thiol molecules in human chronic exposure to aluminum

The physiological role of aluminum (Al) is not yet known. Exposure to Al may cause many human disorders. The aim of this study was to explore how occupational human exposure to Al might affect the body oxidative stress. The relation between Al toxicity and oxidative stress was studied in blood samples obtained from 45 primary Al production workers, with a minimum work history of three years in the age range of 29–52 years. They were evaluated for oxidative stress biomarkers including thiobarbituric acid reactive substances (TBARS) indicator of lipid peroxidation, ferric reducing ability of plasma (FRAP) indicator of total antioxidant capacity, total thiol molecules and Al level in blood. The results showed that workers have significantly higher blood Al levels and concomitant lower blood FRAP and total thiol molecules in comparison to controls. Smokers had lower total thiol molecules than non-smokers. The subjects who had a previous history of disease had lower FRAP levels. It is concluded that Al induces oxidative stress in primary Al production workers. Supplementation of workers with antioxidants may have beneficial effects.     

Effect of Zinc Oxide nanoparticles on cellular oxidative stress and antioxidant defense mechanisms in mouse liver

Zinc oxide nanoparticles (ZnO₂), a common ingredient of cosmetics has a huge variety of applications. Previous studies reported oxidative stress mediated toxicity of ZnO₂ nanoparticles on various mammalian cell lines. Although zinc (Zn) is an essential mineral at higher concentrations this metal is toxic. The present study focused on size determination by monitoring changes in activities of antioxidant defense mechanism in response to oxidative stress induced by ZnO₂ nanoparticles using mouse liver tissue homogenates. The study also investigated effects of oxidative stress induced DNA damage by determining formation of 8-OHdG in mouse liver homogenate. A cytotoxicity assay was also carried out in L929 cells to determine cell viability. The results of the study indicated that 50μg/ml of ZnO₂ nanoparticles induced 50% cell death. Alterations in antioxidant parameters and 8-OHdG were also noted. Data showed that there was a concentration-dependent fall in cell viability, decrease antioxidant enzyme levels and increase formation of DNA adduct (8-OHdG) when mouse liver tissue homogenate were exposed to ZnO₂ nanoparticles.     

Rice seedlings under cadmium stress: effect of silicon on growth,cadmium uptake,oxidative stress,antioxidant capacity and root and leaf structures

In this study, the effect of silicon (Si) addition on cadmium (Cd) toxicity in rice seedlings was investigated. After a series of screening experiments, 50 μmol·L^?1 of Cd and 10 μ mol·L^?1 of Si were selected. Treatment of rice seedlings with Cd (50 μ mol·L^?1) resulted in significant accumulation of this metal in roots and shoots. The data revealed that accumulation of Cd resulted in oxidative stress in rice seedlings as evidenced by increased accumulation of hydrogen peroxide (H₂O₂) and malondialdehyde (MDA; a peroxidation product of lipids). However, addition of Si (10 μ mol·L^?1) together with Cd prevented accumulation of Cd, H₂O₂ and MDA. Antioxidant capacity was decreased by Cd but enhanced by Si addition. Cd decreased the length and frequency of root hairs, stomatal frequency, and distorted leaf mesophyll cells and vascular bundles. However, addition of Si together with Cd reduced these abnormalities. The results showed that addition of exogenous Si protected rice seedlings against Cd toxicity by preventing Cd accumulation and oxidative stress (H₂O₂ and MDA accumulation) by increasing Si accumulation and antioxidant capacity, which maintained the structure and integrity of leaf and root.     

Neurotoxicity and oxidative stress induced by permethrin in gills of the freshwater mussel Unio ravoisieri

Pyrethroids are contaminants found in the aquatic environment, and their toxicological effects on aquatic organisms have received extensive attention. However, the impact on freshwater bivalve of exposure to these chemicals is still largely unknown. Freshwater mussels Unio ravoisieri were exposed to two nominal permethrin (PM) concentrations C1?=?50?µg/L and C2?=?100?µg/L during 7 days. The measured concentrations of PM using gas chromatography (GC/ECD) in the treated aquariums were, respectively, 28.7–62.3?µg/L. Catalase (CAT), Glutathione-S-transferase (GST), and Acetylcholinesterase (AChE) activities, Glutatione (GSH) and Malondialdehyde (MDA) levels were determined in gills of U. ravoisieri. Significant increase in CAT activity by the lowest concentration and decrease by highest concentration were observed. Additionally, GST activity was increased in a concentration-dependent manner. However, statistically significant decrease in GSH levels (about 39%) was observed only at high concentration of this compound (100?µg/L). PM generated an increase in MDA levels reaching the highest value at the high concentration. AChE activity of mussel ranging from 51% inhibition at lowest concentration 50?µg/L to 89% inhibition at highest concentration 100?µg/L. The results indicated that oxidative stress and cell damage might be one of the main mechanisms of PM toxicity to freshwater mussels.     

Subacute chlorpyrifos-induced alterations in serum lipids and some oxidative stress biomarkers in male Wistar rats: beneficial effect of acetyl-L-carnitine

The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg^?1), II (ALC) received ALC (300 mg kg^?1); III (CPF) received CPF (8.5 mg kg^?1 ～ 1/10th LD₅₀); IV (ALC+CPF) was pretreated with ALC (300 mg kg^?1) and then exposed to CPF (8.5 mg kg^?1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.     

Permethrin induced oxidative stress and neurotoxicity on the freshwater beetle Laccophilus minutus

Biomonitoring has become a useful tool in environmental risk assessment of anthropogenic activities releasing disturbing pollutants. Permethrin, used worldwide to control a wide range of pest insects, can threaten aquatic biota, potentially useful as precocious bioindicators in ecotoxicology. This study seeks to assess the acute toxicity permethrin to the freshwater beetle, its availability in water, as well as, its uptake. The acute toxicity of permethrin to non-target species was studied under laboratory conditions to assess its effect, after the exposure 48 h, on the freshwater beetle Laccophilus minitus considering changes in some enzymatic activities; a specific biomarker of neurotoxicity (acetylcholinesterase) and a non-specific biomarker of oxidative stress (superoxide dismutase and catalase). The rates of permethrin in water and insects were determined using gas chromatography. The low measured concentration of the pesticide 0.0013 μg/L didńt modify the SOD and CAT activities in comparison with controls, only the high concentrations (0.023 and 0.18 μg/L) induced a significant increase in the enzyme activity. A similar profile was recorded for the H₂O₂ level. The permethrin treatment induced a drastic depletion of AChE activity. As outcomes, uptake at a low level (<6.8 ± 0.43 ng/g dry weight) showed to be the factor underlying the alterations in the beetles exposed to permethrin. Such findings provide information on the behaviour of permethrin within the environment and its biological target through its neurotoxicity and induction of oxidative stress in a freshwater beetle.     

Protective role of L-ascorbic acid against cypermethrin-induced oxidative stress and lipid peroxidation in Wistar rats

Cypermethrin is a synthetic pyrethroid insecticide used for pest control in agriculture and as an acaricide in man and animals. This study was undertaken with the objective to investigate the propensity of cypermethrin to induce oxidative stress in rats following repetitive dermal exposure and its possible attenuation by L-ascorbic acid. Results obtained showed that cypermethrin significantly (p < 0.05) increased malonaldehyde levels, activity of catalase in rat erythrocytes and plasma protein levels. Whereas, activities of glutathione (GSH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) were significantly (p < 0.05) reduced in the cypermethrin exposed rats as compared to the control. Supplementation of L-ascorbic acid in cypermethrin-exposed rats decreased lipid peroxidation of erythrocytes, total plasma protein and catalase activity significantly (p < 0.05) compared to non-cypermethrin-exposed group. However, L-ascorbic acid did not alleviate the negative effects of cypermethrin on the activities of SOD and GSH. This study revealed that the presence of L-ascorbic acid diminishes the adverse effects of cypermethrin on some oxidative stress parameters.     

The effects of evening primrose oil on arsenic-induced oxidative stress in rats

Forty-eight male Wistar albino rats were allocated to the four groups such that each comprised 12 animals. The first group was maintained as the control. In group 2, evening primrose oil was administered at a dose of 0.1 mL rat^?1 day^?1 (～500 mg kg^?1 bw) into the stomach via gavage, whilst in group 3 sodium arsenide was administered at a concentration of 100 mg L^?1 in ad-libitum drinking water for 30 days. The fourth group was given 0.1 mL rat^?1 day^?1 evening primrose oil into the stomach via gavage plus 100 mg L^?1 of sodium arsenide in ad-libitum drinking water for 30 days. At the end of the 30th day, tissue (liver, lung, kidney, brain, heart, spleen, and testis) and blood samples were collected from each group. Malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase, catalase and glutathione peroxidase activities were measured in the samples. Exposure to arsenic in rats causes oxidative stress by increasing lipid peroxidation (increase of MDA and NO levels) and altering the activity of antioxidant enzymes. Evening primrose oil did not have any adverse effects. Furthermore, it was ascertained that the administration of arsenic with evening primrose oil reduced the severity of oxidative stress.     

环境污染物导致氧化应激的关键信号通路及其检测方法

环境污染物能够以多种途径进入生物体内,在体内产生含氧自由基等活性氧物质,并通过多种信号通路及酶反应引起氧化应激,造成生物体内的脂质过氧化、蛋白质损伤、DNA表达改变、酶失活等,从而引发心血管疾病、风湿类疾病、感染及癌症等的发生。本文对环境污染物致氧化应激产生的原因、涉及的信号通路及酶反应、造成的危害,以及常见的基于细胞模型的氧化应激检测方法进行了综述,期望为评价环境污染物和检测氧化损伤提供参考。     

Protective effect of Tamarindus indica fruit pulp extract on collagen content and oxidative stress induced by sodium fluoride in the liver and kidney of rats

Fluorosis is a serious public health problem in many parts of the world. The generation of reactive oxygen species and lipid peroxidation has been considered to play an important role in the pathogenesis of chronic fluoride toxicity. The present study was undertaken to evaluate the protective effect of Tamarindus indica fruit pulp extract on the collagen content and oxidative stress in liver and kidney of fluoride-exposed rats. The first group served as control. The second group received 200 mg L^?1 of sodium fluoride through drinking water. The third and fourth groups received T. indica fruit pulp extract (200 mg kg^?1 body weight) alone and along with fluorinated drinking water respectively, daily by gavage for a period of 90 days. At the end of the experiment, blood samples were collected from all groups, and liver and kidney samples were taken concurrently. Levels of malondialdehyde and glutathione and the activities of superoxide dismutase and catalase were evaluated in the liver and kidney of experimental rats. Furthermore, level of hydroxyproline and histological examination of liver and kidney along with serum biochemical parameters were evaluated. In conclusion, fluoride was determined to cause adverse effects in rats, and the supplementation of tamarind to these animals alleviated the adverse effects of fluoride.     

Effects of benzo(a)pyrene on blood components,tumor markers,and oxidative status in mice

This study was carried out to investigate the effect of long-term exposure to benzo(a)pyrene (B(a)P) in mice. Hemogram, tumor markers, oxidative status, and B(a)P residues in liver tissue were evaluated. Sixty albino Swiss mice were randomly distributed equally into three groups; the control was given 0.1?mL corn oil once a week for 8 weeks. The other two groups were given 20 and 40?mg B(a)P per kg body weight once a week orally for the same period. B(a)P-treated mice suffered from depression and ascites, and macrocytic normochromic anemia was recorded at the 16th and 30th week. There was marked leukocytosis with lymphocytosis at the early stage of the experiment, followed by leukopenia, lymphopenia, and neutropenia at the end of the experiment. Monocytes and arginase activity were elevated throughout the experiment. Alpha feto-protein was detected only in the experimental groups in the 30th week of the experiment. A marked increase in lipid peroxides associated with a decrease in reduced glutathione and glutathione-S-transferase (GST) activity was observed in liver homogenate of the B(a)P-exposed animals. Residues of B(a)P were detected in liver tissue with a concentration parallel to the B(a)P dose level. In conclusion, B(a)P caused abnormal changes in the hemogram, evidence of tumor formation through B(a)P-induced oxidative stress, and it was accumulated in the liver tissue of mice.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

Induction of oxidative stress by benzo(a)pyrene in the epididymis of Wistar rats

The present study was undertaken to evaluate the effect of sub-chronic exposure to benzo(a)pyrene on the antioxidant system and histology of rat epididymal sperm. Intraperitoneal administration of benzo(a)pyrene to male Wistar rats at doses between 1 and 100 µg/kg body weight for 60 days entailed a decrease in the weight of the epididymis (caput and cauda), seminal vesicle, and prostate, while the body weight was not affected. Epididymal sperm reserves were reduced in a dose-dependent manner. Indicators of lipid peroxidation were increased while activities of superoxide dismutase and catalase in all three epididymal regions decreased. Histological malformations were observed in the epididymis. Exposure to benzo(a)pyrene deranges the antioxidant defense system and induces histological changes in the epididymis.     

Implications of oxidative stress in occupational exposure to lead on a cellular level

The aim of this study was to determine oxidative alterations leading to cellular dysfunctions in Pb-exposed subjects by evaluating damage to all major classes of biomolecules in the cell, lipid peroxidation, protein and DNA damage and determine relationships between parameters of Pb toxicity and specific biomarkers of oxidative damage.

Analysis was conducted of smelter workers with high blood Pb and urine aminolevulinic acid levels and slightly elevated values of coproporphyrin and erythrocyte protoporphyrin IX. Significant decreases of thiol groups and increases in carbonyl groups as protein degradation end products, and of nitrite were detected. Elevated rates of lipid peroxidation and rises in the activities of the antioxidant enzymes Cu–Zn superoxide dismutase and catalase were also observed. Both enzymes showed positive correlations with the blood lead levels and urine coproporphyrin, while thiol groups correlated negatively with the same indices. The genotoxic potential of lead was manifested through an increased number of DNA-damaged cells. Increased activities of serum lactate dehydrogenase isoenzymes indicated cellular damage in the lungs, kidneys, and liver. These lead-induced impairments should be taken into consideration in the assessment of Pb-related health hazards.     

Determination of oxidative stress markers and serum cholinesterase among pesticide sprayers in southern Brazil

Small farmers generally spray pesticides manually and often do not use complete protective equipment. The standard test to detect pesticide exposure, which may be associated with toxicity, is the determination of serum cholinesterase, but in chronic exposure to low doses, this test is less sensitive. In this study, in a group sampled among pesticide sprayers without signs of intoxication, cholinesterase, thiobarbituric acid reactive substances (TBARS), catalase (Cat), and superoxide dismutase (Sod) activities were analyzed. Cholinesterase activity was only slightly lower in the farmer group in relation to the control group. However, TBARS and Cat activities were 3-fold increased in the farmers in comparison to the controls. Sod activity was similar in both groups. The group of pesticide sprayers that did not use the complete protective equipment presented a significantly higher level of TBARS than the group that used the complete protective equipment. Therefore, the determination of TBARS and catalase can be useful to identify individuals that are chronically exposed to low doses of pesticides.