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.     

Comparative studies of liver and brain glycogen content of male and female Clarias batrachus (L.) after exposure of different doses of arsenic

Different doses of arsenic (As) were used to investigate comparative toxicity on the liver and brain glycogen content on male and female Indian catfish Clarias batrachus (L.). As-induced effects were associated with gender, dose (5, 10, or 15?mg?L^?1), and varying time periods (48, 96, or 144?h). It was noted that As produced dose- and time-dependent liver glycogenolysis and late brain glycogenolysis. Liver glycogenolysis was significantly increased after 48?h at all three As doses. At the highest dose 15?mg?L^?1, liver glycogen were markedly diminished at in both male and female fish, but in females more reduction was observed than in males. However, with brain glycogen, the significant decrease was noted at 144?h with all three dose levels in both genders, with male being more susceptible. Thus, this study indicates that As produces glycogenolysis. The reduction in the liver glycogen content was more pronounced in female than in the male fish, whereas brain glycogen content decrease was more prominent in males.     

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.     

Influence of marine alga against mercury-induced biochemical changes,structural destabilization,and genotoxicity in marine tiger fish,Therapon jarbua

This study elucidated the protective role of alga against mercury (Hg)-induced toxicity in marine fish. Bath immersion with mercury chloride (HgCl) [0.125 and 0.25?ppm] in combination with the algal extract (3?ppm) to Therapon jarbua offered a significant protection against Hg only induced disturbed liver function, damaged histoarchitecture, elevated oxidative stress, and DNA fragmentation of tissues. Mercury exposure decreased hepatic superoxide dismutase (SOD), catalase (CAT) activities, and the level of nonprotein-soluble thiol (NPSH, GSH), with a concomitant increase in thiobarbituric acid reactive substances (TBARS) in the gill, kidneys, liver, and blood. Algal supplementation diminished the rise in TBARS restoring CAT, SOD, and GSH levels to control. Reduced generation of free radicals may be correlated to protect DNA stability and morphology. This study indicates the ability of alga to ameliorate Hg-mediated injuries. In conclusion, Kappaphycus alvarezii extract did not show any toxicity and its safety is suggestive for using as a supplement in fish food.     

Effects of Selenium Supplementation on Arsenism: An Intervention Trial in Inner Mongolia

This paper reports the effects of a placebo-controlled Se-enriched yeast supplementation trial, conducted for 14 months, on arsenism in adult farmers living in a rural community in Inner Mongolia, China. The farmers had been naturally exposed to elevated concentrations of As in drinking water from tube-wells since 1983 but changed to arsenic-free drinking water when the trial began in June 1996. Blood and hair Se and As concentrations were analysed pre-intervention and at the end of the 3rd, 9th and 14th month, while skin lesions were assessed pre-intervention, as well as at the end of the 14th month, using the Arsenism Clinical Criteria established by the Ministry of Health, China. As the trial was a voluntary one, a number of farmers did not routinely have their blood and hair samples taken for analysis. Consequently, the data have been analysed in two categories. Fifty-four farmers from the Se-group and 29 from the placebo-group who were sampled on each occasion were considered as one group, which has been compared with the second group comprising up to a total of 100 farmers in the Se-group and 86 in the placebo-group. Results calculated for those farmers who were sampled on each occasion, showed that at the end of the trial, blood and hair Se concentrations of the Se-group increased from 0.130 to 0.186 µg ml^–1 and from 0.431 to 0.502 µg g^–1, respectively, while those of the placebo-groups remained constant. Blood and hair As concentrations of the Se-group decreased from 0.051 to 0.015 µg ml^–1 and from 2.57 to 0.680 µg g^–1, respectively, a greater reduction than those in the placebo-group that went from 0.064 to 0.024 µg ml^–1 and from 2.62 to 1.25 µg g^–1, respectively. When the data from all patients were examined, the analytical trends were similar. An evaluation of skin lesions in the category who were sampled for hair and blood on each occasion showed that 41.2% of hyperkeratosis, 50.0% of depigmentation and 44.7% of pigmentation in the Se-group improved one or more degrees, while those in the placebo-group improved by only 7.1, 12.0 and 6.7%, respectively. A total of 61.1% of the adults in Se-group improved in one or more type of skin lesion, but only 17.2% improved in the placebo-group. Comparable results were obtained when all the data from both categories of farmers were examined. Results from the trial showed that Se supplementation was more effective for the improvement of adults who were affected by double or triple skin lesions. In the placebo-group, most of the severely affected adults improved in only one kind of skin lesion, but in the Se-group, more adults improved in two or three kinds of skin lesions. Although the trial was limited by its relatively small size, the results have provided some evidence of the usefulness of Se supplementation for people affected by arsenism.     

Antioxidant enzymes and compounds complement each other during arsenic detoxification in shoots of Isatis cappadocica Desv.

Isatis cappadocica has been reported to be an arsenic (As) hyperaccumulator. Antioxidant enzymes and compounds have been proposed to play an important role in the detoxification and tolerance of As. In the present study, As-induced oxidative stress and antioxidant responses were investigated on I. cappadocica grown hydroponically in response to application of arsenate (0–1200?μmol). As accumulation increased with an increase in arsenate concentration in the medium. Along with a significant increase in arsenate concentration, a build up in hydrogen peroxide, indicators of oxidative stress, was observed. The activity of superoxide dismutase and peroxidase was induced after arsenate treatment, reached a maximal value at 800?μmol arsenate and then declined at the highest arsenate treatment. Glutathione reductase activity and contents of non-enzymatic antioxidants (carotenoids, flavonoids and anthocyanins) increased significantly as arsenate concentration augmented. These results indicated that high efficient antioxidant system may play significant roles in As detoxification and improve I. cappadocica tolerance against As toxicity.     

The usability of oxidative stress and detoxification biomarkers in Gammarus pulex for ecological risk assessment of textile dye methyl orange

The present study was undertaken to determine the toxicity of the methyl orange by using the changes of some antioxidant and detoxification enzyme activities in Gammarus pulex. Lethal Concentration (LC) value of Methyl Orange (MO) was determined. Three sublethal doses of MO (1/4; 1/8 and 1/16 of LC value) were exposed to G. pulex for 24 and 96?h. Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GSH-P_X), Cytochrome p450 (CYP1A1), Glutathione S-transferase (GST) activities as well as Glutathione (GSH) and Malondialdehyde (MDA) levels were determined by using The enzyme-linked immunosorbent assay (ELISA) kit. The CAT and CYP1A1 activities were decreased in all the groups exposed to different doses of MO. GST activity and GSH, MDA levels were increased all the groups exposed to different doses of MO. The GSH-P_X activities were changed in all the groups. MO affected SOD activity at different levels and in different concentrations. In our study, it has been found that exposure duration didn’t significantly affect the biochemical biomarkers except for GST and GSH. In conclusion, alterations in antioxidant and detoxification enzymes and lipid peroxidation may potentially be used as sensitive biomarkers for risk assessment of dyes in the environment and may contribute to the establishment of discharge regulations.     

Effects of selenium on activity of glutathione peroxidase and expression of selenium metabolism-related genes in Brassica

Inorganic selenium (Se) is absorbed and enriched by plants and converted into a stable and nutritionally important organic form, which subsequently when consumed by humans or animals results in increased Se tissue levels. Brassica is one of the most potent Se-enriched plants. The aim of this study was to compare differences in Se enrichment between two predominant Brassica plants namely Brassica rapa Linn L. and Brassica tumida Tsenet Lee L. on Se metabolic parameters. Plants exposed to soil Se levels (0, 0.5, 1, 2.5 or 5?mg/kg) were examined on the activity of glutathione peroxidase (GSH-Px), Se levels and expression of Se metabolism related genes using soil pots. Data showed that activities of GSH-Px in leaf and root of the two Brassica species were significantly increased in the presence of Se at 2.5?mg/kg. Se concentrations of leaf, stem and root in B. tumida Tsenet Lee L. and B. rapa Linn L. rose from 0.31 to 21.84-fold (leaf), 1.15 to 15.16-fold (stem) and 2.11 to 15.26-fold (root) in the presence of metal in a concentration-dependent manner. The highest expression levels of adenosine triphosphate (ATP), ATP sulfurylase (APS), selenocysteine methyltransferase (SMT), serine acetyltransferase (SAT), cysteine desulfurase (CysD) and S-adenosyl-l-Met:l-Met S-methyltransferase (MMT) in leaf of B. rapa Linn L. were found at 1?mg/kg Se. The highest expression levels of ATP, APS, SMT, SAT, CysD and MMT in leaf of B. tumida Tsenet Lee L. were observed at 2.5?mg/kg Se. The Se concentrations in leaf, stem and root of B. rapa Linn L. were higher than in B. tumida Tsenet Lee L. under the same soil Se level conditions. At the same Se level, differences in the expression of Se-related genes were observed between these two Brassica species. Our observations may be used to optimize the utilization of Brassica as a nutritional source of Se by growing this plant under certain soil conditions.     

Hepatoprotective effects of taurine against mercury induced toxicity in rats

An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline phosphatase(ALP) in serum and lipid peroxidation (LPO) in liver tissue significantly increased whereas Glutathione (GSH), Glutathione peroxidase(GPx), Catalase (CAT) and Superoxide dismutase (SOD) were simultaneously decreased in the liver tissue. Present results indicate that the liver tissue was completely damaged, after mercury treatment. In another group of animals, taurine (5 mg/kg body wt.) was administrated for another 15 days. Taurine administration was observed to improve the liver function in mercury intoxicated animal as indicated by the decline in increased levels of AST, ALT and ALP in serum and LPO content in liver tissue. The decreased level of antioxidant system (GSH, GPx, CATand SOD) has been promoted Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.     

Lead-induced alterations in protein-deficient rat liver–role of zinc

This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227?mg?L^?1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100?mg?kg^?1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated PD rats. In contrast, serum AST activity was elevated both at 3 and 8 weeks while serum ALT activity was elevated at 8 weeks in Pb-treated PD rats. Pb treatment to PD rats elevated hepatic ALP, AST and ALT activities but depressed hepatic AST. Zn supplementation to Pb-treated PD rats restored the altered enzyme activities. The levels of K, Fe, Cu, Zn, Se and Rb were altered in protein deficiency. Furthermore, treatment with Pb to these animals depressed the Cu levels. Zn treatment to Pb-treated PD animals tended to restore the levels of altered elements. Hence, the present study clearly suggests that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.     

Low levels of lead and glutathione markers of redox status in human blood

Exposure to lead (Pb) is implicated in a plethora of health threats in both adults and children. Increased exposure levels are associated with oxidative stress in the blood of workers exposed at occupational levels. However, it is not known whether lower Pb exposure levels are related to a shift toward a more oxidized state. To assess the association between blood lead level (BLL) and glutathione (GSH) redox biomarkers in a population of healthy adults, BLL and four GSH markers (GSH, GSSG, GSH/GSSG ratio and redox potential E _h ) were measured in the blood of a cross-sectional cohort of 282 avid seafood-eating healthy adults living on Long Island (NY). Additionally, blood levels of two other metals known to affect GSH redox status, selenium (Se) and mercury (Hg), and omega-3 index were tested for effect modification. Regression models were further adjusted for demographic and smoking status. Increasing exposure to Pb, measured in blood, was not associated with GSSG, but was associated with lower levels of GSH/GSSG ratio and more positive GSH redox potential E _h , driven by its association with GSH. No effect modification was observed in analyses stratified by Hg, Se, omega-3 index, sex, age, or smoking. Blood Pb is associated with lower levels of GSH and the GSH/GSSG ratio in this cross-sectional study of healthy adults.     

Protective effects of quercetin against sodium fluoride-induced oxidative stress in rat erythrocytes

Protective effects of quercetin against oxidative stress induced by sodium fluoride intoxication in rat erythrocytes were evaluated. Rats were divided into five groups consisting of 10 in each for this experiment. The animals of group I received water and standard diet to serve as control group, the animals of groups II and III were treated with quercetin (10 and 20?mg?kg^?1 body weight), administrated intraperitoneally for 7 days followed by sodium fluoride (600?ppm) in drinking water for the next 7 days. The animals of group IV were treated with vitamin C (10?mg?kg^?1) intraperitoneally for 7 days followed by sodium fluoride treatment for next 7 days serving as positive control group. The animals of group V were treated only with sodium fluoride (600?ppm) for the same time and were used as control group. Blood sample were collected via retro-orbital puncture. The antioxidant enzymes, superoxide dismutase, and catalase, as well as the levels of reduced glutathione and lipid peroxidation end products were measured in erythrocytes. There was a significant increase in lipid peroxidation along with a decrease in superoxide dismutase activity in the erythrocytes of sodium fluoride-treated animals. Quercetin treatment prior to fluoride administration normalized the levels of all parameters measured in the rat erythrocytes.     

Ameliorated effects of garlic (Allium sativum) on biomarkers of subchronic acrylamide hepatotoxicity and brain toxicity in rats

Acrylamide (ACR) exerts its toxicity through stimulation of the oxidative stress; yet, its effect on neurotransmitter catabolic enzymes has not been elucidated. We investigated the effects of ACR exposure on brain and hepatic tissues antioxidant enzymes activities and different markers such as, acetylcholinesterase (AChE), nitric oxide (NO), monoamine oxidase (MAO), and lipid profile, and to evaluate the protective effects of garlic against ACR toxicity. Male Sprague-Dawley rats were exposed to ACR (1 mg kg^?1 body weight) with or without diet containing 1.5% of garlic powder for 40 days. ACR administration showed a decrease in AChE activity associated with an increase in MAO activity in both brain and hepatic tissues. In addition, ACR administration increased the lipid peroxidation and NO levels of both tissues while decreased the activities of glutathione (GSH), superoxide dismutase, and glutathione-S-transferase (GST). On the other hand, the activities of glutathione peroxidase (GPx) and catalase activities increased as a consequence of GSH depletion after ACR exposure. Finally, ACR exposure increased the brain and liver lipid profile of cholesterol, triglycerides and total lipid, while phospholipids level was decreased. Coadministration of garlic powder with ACR significantly attenuated oxidative stress, MAO activity, and inflammation in brain and hepatic tissues but did not ameliorate AChE activity. In conclusion, our results emphasized the role of garlic as a potential adjuvant therapy to prevent ACR neurotoxicity and hepatotoxicity.     

Vitamin E-mediated protection on methomyl-induced alterations in rat liver

The present study was carried out to observe the possible beneficial effects of Vitamin E, a natural antioxidant on methomyl-induced biochemical and histological alterations in rat liver. To carry out the investigations, animals were segregated in four different groups. Animals in Group I served as normal controls. Animals in Group II were given single methomyl dose orally in water (9 mg kg^?1 b.wt). Animals in Group III were injected intraperitoneally with Vitamin E (50 mg kg^?1 b.wt) for 1 week on alternate days. Animals in Group IV were administered Vitamin E 1 week before subjecting them to methomyl treatment. Animals in all the groups were sacrificed 24 h after the end of treatments. Different biochemical estimations were carried out, which included estimation of aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), alkaline phosphatase (ALP) and acetylcholinesterase (AChE). Further, to examine the oxidative damage lipid peroxidation (LPO) and glutathione (GSH) levels as well as antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSHPx), and glutathione-6-phosphate dehydrogenase were estimated in liver samples. AchE activity was inhibited significantly both in serum and liver following methomyl treatment. Administration of methomyl caused a significant increase in serum AST, ALT and ALP which indicated hepatic damage. LPO was found to be significantly increased, whereas GSH levels were decreased in the liver of methomyl-treated animals. The activities of SOD and catalase were significantly decreased whereas GST and GSHPx activities were found to be elevated significantly following methomyl treatment. No significant change in the enzyme activity of GR and glutathione-6-phosphatase dehydrogenase was observed after methomyl treatment. Vitamin E supplementation was able to attenuate appreciably the methomyl-induced changes in LPO levels along with SOD and GST activities. Histopathological studies following methomyl treatment revealed that hepatocytes, were not very well delineated and nuclei showed degenerative changes. Whereas, following Vitamin E supplementation in combined treatment group nuclei showing degenerative changes become less in number. The study, therefore, concludes that Vitamin E has a potential in mitigating most of the adverse effects induced by methomyl acute toxicity.     

不同价态无机砷对罗非鱼肝脏砷积累及GSH/GST解毒代谢的影响

低剂量中长期暴露下的氧化胁迫是砷对水生生物致毒的重要机制之一。本文通过对罗非鱼进行32 d的食物相砷暴露,测定不同时间点罗非鱼肝脏中谷胱甘肽(glutathione,GSH)含量和谷胱甘肽巯基转移酶(glutathione S-transferase,GST)活性,揭示不同价态无机砷对罗非鱼肝脏中GSH/GST的影响机制。经三价砷(As(III))暴露后,砷含量在2 d内显著增加而在随后的30 d内无显著性差异; 0～2 d内GSH含量显著增加,后降低,13 d后GSH含量均低于空白组; 0～6 d GST活性均大于空白组,6～8 d GST活性降低,8 d后活性高于空白组,且32 d达到最大值。经五价砷(As(V))暴露后,罗非鱼肝脏中砷含量逐渐增加,在20 d时达到最大值而后无显著性差异; 0～2 d时GSH含量降低,随后逐渐增加,在16 d达到最大值,16 d后GSH含量均低于空白组; 0～8 d时GST被大量诱导合成,8～20 d时GST合成被抑制,20 d后活性增加,在32 d达到最大值。As(III)和As(V)对罗非鱼GSH/GST的不同影响与其在罗非鱼体内的积累量有关。As(III)暴露后各时间点罗非鱼肝脏中的砷含量与GSH含量呈统计学正相关,而As(V)暴露无明显相关性。这是因为As(V)进入罗非鱼肝脏后会还原为As(III),进而GSH作为可提供巯基的还原剂而被大量消耗。另外,As(III)暴露后各时间点罗非鱼肝脏中的砷含量与GST活性呈显著负相关,而As(V)暴露却呈现出很强的滞后性,这是由于进入生物体内的As(V)需转化为As(III)后,才可直接作用于酶系统。可见,不同形态砷对水生生物的致毒机制需进一步深入研究。     

Influence of diet,vitamin, tea,trace elements and exogenous antioxidants on arsenic metabolism and toxicity

Health risk of arsenic (As) has received increasing attention. Acute and chronic exposure to As could cause several detrimental effects on human health. As toxicity is closely related to its bioaccessibility and metabolism. In real environment, many factors, such as diet and nutrition, can influence As bioaccessibility, metabolism and toxicity. This paper mainly reviews the influences of diets and elements on As bioaccessibility, metabolism and toxicity and their underlying mechanisms to provide suggestions for future investigations. Vitamins, jaggery, fruit, tea, glutathione, N-acetylcysteine and zinc could reduce the As-induced toxicity by increasing antioxidative enzymes to antagonize oxidative stress caused by As and/or increasing As methylation. However, bean and betel nut could increase risk of skin lesions caused by As. Interestingly, high-fat diet, selenium and iron have incompatible effects on As bioaccessibility, metabolism and toxicity in different experimental conditions. Based on current literatures, the As methylation and As-induced oxidative damage might be two main ways that the diets and elements influence As toxicity. Combined application of in vitro human cell lines and gastrointestinal models might be useful tools to simultaneously characterize the changes in As bioaccessibility and toxicity in the future research.     

Selenium and arsenic content of agricultural soils from Bangladesh and Nepal

Arsenic (As) contamination of the available domestic drinking water from shallow aquifers to villagers in Bangladesh often exceeds the newest WHO standard of <10 µg As L^?1 and the older Bangladeshi standard of <50 µg As L^?1. An estimated 9.2 million shallow tube wells in Bangladesh deliver water to 97% of the rural population, placing an estimated 57 million people at risk for arsenicosis. The contamination of drinking water by As extends to W. Bengal, India and Nepal. The same shallow aquifers used for domestic water are also used to irrigate food crops, particularly rice. Irrigation adds As to soils and increases exposure of the population to additional As via foods consumed. Selenium (Se), an essential trace mineral found in soils, is absorbed by plants, entering the human food chain. It was suggested that a low dietary intake of Se may be contributing to the problem of human arsenicosis in Bangladesh. Dietary Se acts as a natural antidote to As by (1) accelerating As excretion, (2) sequestering As by complexation and (3) as an antioxidant component of the enzyme glutathione peroxidase that may counteract the prooxidant effects of As that contribute to arsenicosis and cancer. Analysis of 70 agricultural soil samples from Bangladesh by fluorimetry, ICP-AES and Neutron Activation Analysis showed the soils analyzed to be high in As (～33 µg g^?1) and biologically low in soluble Se (～0.02 µg g^?1). A low dietary intake of Se related to low soil content and this mineral in foods may be contributing to human arsenicosis in the Ganges–Brahmaputra delta.     

汞、硒暴露对紫贻贝(Mytilus edulis)抗氧化酶系统的影响

为了研究重金属汞及微量元素硒对海洋贝类的毒性效应,揭示汞、硒在生物体内的相互作用机制,用汞和硒对指示生物紫贻贝(Mytilus edulis)进行单一及联合亚慢性暴露实验。设置对照组(0μg·L-1)、汞暴露组(25μg·L-1Hg2+)、硒暴露组(4μg·L-1Se4+)以及硒汞联合暴露组(25μg·L-1Hg2++4μg·L-1Se4+)4个实验组,并分别在暴露期间的第0、2、4和6天定时采集样本,测定紫贻贝鳃SOD、GPx及CAT3种抗氧化酶活性。将实验数据进行ANOVA分析处理后,结果表明:与对照组相比,汞暴露组SOD和GPx均呈现先显著升高(p<0.05或p<0.01)后降低(p<0.01或p<0.001)的趋势,CAT则从第4天开始显著降低(p<0.05);硒暴露组中SOD活性始终高于对照组(p<0.001),GPx活性在第2天也显著升高(p<0.001),CAT活性始终与对照组相近;硒汞联合作用与汞暴露组相比,SOD、GPx和CAT活性在不同时间点均有显著升高(p<0.05),而与硒暴露组相比,3种酶活性均低于硒单独暴露的水平。说明汞在短期能够诱导抗氧化酶活性,随着暴露时间的延长,则表现出明显的抑制作用;微量硒能够增强抗氧化酶系统活性,对汞导致的氧化损伤具有拮抗作用。     

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.     

Evaluation of initiation activity of dimethylarsinic acid: Initiation potential of rat hepatocarcinogenesis

There is a dearth of data on the initiation activity of dimethylarsinic acid (DMA (V)), a major metabolite of the ubiquitous environmental and occupational carcinogen and toxicant, arsenic (As). The initiation activity of DMA (V) was investigated on rat hepatocarcinogenesis with liver being a major target organ for As-induced carcinogenicity. A total of 50 rats at 10 weeks old were randomly divided in a nine-week medium-term bioassay into four groups. Groups 1 and 2 received 200 ppm of DMA (V) in drinking water for four weeks while groups 3 and 4 drank only tap water until the sixth week when groups 1 and 3 were given 0.01% 2-acetylaminofluorene (2-AAF) in their diet for two weeks in the promotion stage. All animals were subjected to two-third partial hepatectomy (PH) at the seventh week. Quantitative analysis of glutathione S-transferase placental form (GST-P) positive foci in liver, a pre-neoplastic marker of rat hepatocarcinogenesis, demonstrated higher numbers in group 1 (DMA (V) + 2-AAF) than 3 (2-AAF alone) at foci consisting of two–four cells and 15 or a greater number of cells. The numbers of GST-P positive foci consisting of five–nine cells were significantly higher in group 1 than 3. Foci consisting of 10–14 cells were also higher but not significantly different. The GST-P positive foci were apparently similar in groups 2 and 4. Expression of total GST-P positive foci was significantly higher in group 1 compared to 2, 3 or 4. The proliferating cell nuclear antigen (PCNA) test performed to clarify the apparent trend of GST-P data revealed significantly higher PCNA index in group 1. Data indicate weak initiation potential of DMA (V) and for the first time appear to provide evidence for initiation activity in DMA (V)-induced hepatocarcinogenesis in rats.