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.     

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.     

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     

The role of thymoquinone as antioxidant protection on oxidative stress induced by imidacloprid in male and female Swiss albino mice

The aim of the present study was to evaluate the possible protective effects of thymoquinone (TQ), an antioxidant agent, against imidacloprid (IMI)-induced oxidative stress in male and female mice. In total, 48 Swiss Albino male and female mice were fed a standard rodent diet and divided into 3 equal groups: the animals in the control group (vehicle treated) were given corn oil, the second group were orally administered 15 mg/kg/day IMI alone, and the third group were orally administered 15 mg/kg/day IMI and with TQ at 10 mg/kg/day for 21 days. During the experimental period, there were no significant changes between initial body weights and final body weights of IMI treated male and female mice. IMI produced significant increase in blood, liver, kidney, and heart malondialdehyde (MDA) levels and decrease in blood and liver glutathione (GSH) levels. In addition, IMI treatment decreased erythrocyte, liver, and kidney superoxide dismutase (SOD) activity in male mice and decreased erythrocyte and liver SOD activity in female mice. Erythrocyte catalase (CAT) activities were found to be low in male and female mice. However, treatment with TQ reversed IMI-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. Moreover, TQ exhibited protective action against the IMI-induced histopathological changes in tissues of male and female mice. In conclusion, TQ was found to be effective in protecting mice against IMI-induced oxidative stress by enhancing antioxidant defense mechanisms.     

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.     

Chlorpyrifos induces oxidative stress in rats

This study was carried out in male Wistar rats to determine the potential effects of chlorpyrifos (CHP) on oxidative stress, as was reported for organophosphorus (OP) pesticides. Following an acute, daily 3- or 14-day exposure with CHP at doses of 2.5, 5, or 25 mg kg^?1 data showed significant increases in malondialdehyde levels at both exposure durations and at all doses, except for 2.5 mg kg^?1, in hepatic and aorta, kidney, and plasma samples. The nitrites (NO) showed elevation at 25 mg kg^?1 in aorta, at 3- and 14-day exposure, in hepatic tissue with all doses at 3-day exposure, but not at 14-day with a 5 mg kg^?1 dose. In plasma, increases occurred only at 25 mg kg^?1 at both exposure times, and in kidney at all doses and both exposure durations. Superoxide dismutase (SOD) enzyme activity in the aorta sample was statistically significant at all doses at 3 days and at 14 days, except at 2.5 mg kg^?1; and in hepatic tissue only at 25 mg kg^?1 dose at both durations. In plasma SOD activity was elevated at all doses at 3 days, but at 14 days only at 25 mg kg^?1. Data suggests that oxidative stress may be involved in the effects of CHP on rats.     

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.     

Oleuropein alleviates malathion-induced oxidative stress and DNA damage in rats

The effects of acute exposure to 250 mg/kg malathion and the protective effects of 20 mg/kg oleuropein, both administered intraperitoneally, were evaluated in Wistar male rats. Malathion administration increased malondialdehyde, nitric oxide, 8-hydroxy-2′-deoxyguanosine, total oxidant status, and DNA damage, yet decreased total antioxidant activity, superoxide dismutase, and catalase activities in blood, liver, and kidney. Administration of oleuropein reversed malathion-induced oxidative stress, lipid peroxidation, DNA damage, and antioxidant enzyme activity.     

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.     

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.     

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.     

Antimony induces oxidative stress and cell death in normal hepatocytes

Antimony (Sb) accumulates in the liver which is one of the target organs for metal-mediated toxicity. Although toxicity of Sb was previously investigated, the precise mechanism of Sb-induced hepatotoxicity remains to be determined. The aim of this study was to examine the role of oxidative stress, and mitochondria in the induction of cell death by Sb. Our results showed that liver cell lysis induced by Sb is mediated by reactive oxygen species (ROS) formation, lipid peroxidation and decline of mitochondrial membrane potential (MMP). Antimony-induced ROS formation, lipid peroxidation and reduction of MMP were significantly diminished by antioxidants and ROS scavengers such as dimethyl sulfoxide and mannitol; mitochondrial permeability transition (MPT) pore sealing agents such as carnitine and trifluoperazine; and adenosine triphosphate (ATP) generator, L-glutamine. Antimony-induced ROS formation, lipid peroxidation and fall in MMP were potentiated by glutathione (GSH) depletion via n-bromoheptane. MPT pore sealing agents and ATP generator inhibited hepatotoxicity, indicating Sb-activated cell death via mitochondrial pathway. Pretreatment of hepatocytes with antioxidants and ROS scavengers also blocked cell death induced by Sb, whereas GSH depletion enhances Sb-induced cell death, suggesting that oxidative stress may be directly involved in the reduction of MMP. These findings contribute to a better understanding of the mechanisms that mediate Sb-induced cell death in isolated rat hepatocytes.     

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.     

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.     

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.     

Influence of hypothyroidism on oxidative stress,c-Fos expression,cell cycle,and apoptosis in rats testes

The molecular basis of male reproduction for cross-regulation between androgen and thyroid hormone axes is still rudimentary. This study aims to define a possible mechanism of hypothyroidism-induced reproductive influence with respect to sex hormone, mineral, sperm motility, oxidative stress, c-Fos expression, cell cycle, and apoptosis in rat testes. The Wistar rats were randomly divided into control group (NS) and hypothyroidism group [1 ml/100g BW/day, 0.1% propylthiouracil (PTU)] by intragastric gavage for 60 days. Blood samples were collected to measure the serum levels. The epididymis was excised to measure sperm motility and testes were excised to measure mineral, oxidative stress, c-Fos expression, cell cycle, and apoptosis. After 60 days, body weight, relative testes weight, triiodothyronine, and total thyroxine were all significantly decreased, whereas thyroid stimulating hormone was increased in the hypothyroidism group. A significant increase in sex hormone level of estradiol (E2) and significant decreases in testosterone (T) and T/E2 ratio were observed following PTU treatment. And sperm quality was also significantly changed. There were significant decreases in the contents of calcium (Ca²⁺) and zinc (Zn²⁺). On the other hand, malondialdehyde and hydrogen peroxide contents significantly increased, whereas the activity of superoxide dismutase, catalase and nitric oxide synthase and nitric oxide content significantly decreased in hypothyroid rats. The mRNA and protein expressions of c-Fos decreased significantly. The cell percentage in G0/G1 phase increased significantly, whereas decreased significantly in S and G2/M phases. Also, a significant increase in testicular cell apoptosis was observed in hypothyroid-treated rats. These results suggested that hypothyroidism could affect reproductive function in the form of changed sex hormone levels, sperm motility and testicular Ca²⁺ and Zn²⁺, and enhanced oxidative stress leading to c-Fos abnormal expression and increased apoptosis.     

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.     

Effect of formaldehyde exposure on structure and function of epididymis in adult rats: a histological and biochemical study

Formaldehyde (FA), a ubiquitous environmental pollutant, is extensively used in hospitals, laboratories, and industrial settings. Previous studies showed that FA exerts adverse effects on testicular function and as epididymis is known to play an important role in the maturation and storage of sperm, the effects of FA were examined on epididymis. In particular, this study was designed to investigate the influence of FA on structure and function of epididymis in adult male rats using histological and biochemical methods. Sprague-Dawley adult rats were randomly allotted to three groups and exposed to FA at a 0 (control), 0.5, or 10 mg m^?3 by inhalation for 28 days. The results indicated that epididymal toxicity of FA was concentration dependent. Epdididymal structure and function in rats of 0.5 mg m^?3 FA exposure group showed no apparent difference from control. However, epididymal weight, sperm count and motility, the activities of superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were significantly decreased, whereas the levels of malondialdehyde (MDA) was significantly increased in epididymis of rats exposed to 10 mg m^?3 FA. Moreover, microscopy with hematoxylin and eosin (H&;E) staining showed atrophy of epididymal tubules, disintegration of epididymal epithelium, disorganization, and even vacuolar denaturalization of epididymal epithelial cells. There was hyperemia in interstitial vasculature and lumina were oligozoospermic in rats of 10 mg m^?3 FA exposure group. In conclusion, FA exposure alters the epididymal structure and function by inducing oxidative stress in epididymis of adult rats.     

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 cimetidine and N-acetylcysteine on paraquat-induced acute lung injury in rats: a preliminary study

Abstract

Lung injury in rats challenged with paraquat at 20?mg kg^?1 body weight was histopathologically evident by inflammation, hemorrhage, and vascular congestion. Increased levels of reactive oxygen species and lipid peroxidation, decreased glutathione content, and lower tissue antioxidant capacity was found. The effects of N-acetylcysteine and cimetidine, a well-known potent inhibitor for organic cation transport, were examined. Lung injury was attenuated by N-acetylcysteine but not by cimetidine. The findings are consistent with the assumption that beneficial effects of N-acetylcysteine administration in paraquat-challenged animals might be linked to its ability for preserving the cellular redox environment and preventing oxidative stress, while cimetidine might even hasten paraquat-induced lung injury. On the other hand, the effects of cimetidine on paraquat-induced lung injury underline the importance of future studies on the role of transporters in this complication.