Oxidative stress indices and plasma biochemical parameters during oral exposure to arsenic in rats

Nandi, Dilip Kumar; Patra, R. C.; Swarup, D.

doi:10.1016/j.fct.2006.04.013

Cited by 87 publications

(45 citation statements)

References 27 publications

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“…This might also support a hypothesis that by increasing the antioxidant capacity of cells may lead to a long-term more effective treatment of arsenic poisoning [16,17]. This strategy can be effective if we (1) either reduce the possibility of interaction of metal with critical biomolecules leading to oxidative damage or (2) by supplementation of an endogenous antioxidant, which will bolster the cells antioxidant defenses [7,10,18]. Although the fact that arsenic induces oxidative stress is now well established and well reported, the usefulness of antioxidants alone or in conjunction with chelation therapy has recently been reported to be a better treatment option to achieve the optimum effect of chelation therapy [15,19,20].…”

Section: Introductionmentioning

confidence: 80%

“…Toxicity of arsenic (III) has been suggested due to (1) its direct binding with -SH groups or (2) indirectly through generation of reactive oxygen species (ROS) [7,8]. The toxicity of inorganic arsenic appears to be mediated through its ability to substitute phosphate groups, affecting enzymes that depend on this group for their activity (e.g., interfering in the synthesis of ATP and DNA).…”

Section: Introductionmentioning

confidence: 99%

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Quercetin Administration During Chelation Therapy Protects Arsenic-Induced Oxidative Stress in Mice

Mishra

Flora

2008

Biol Trace Elem Res

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We studied the efficacy of quercetin and a thiol chelating agent, monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA) either individually or in combination against arsenic-induced oxidative stress and mobilization of metal in mouse. Animals were chronically exposed to 25 ppm arsenite as sodium arsenite in drinking water for 12 months followed by treatment with MiADMSA (0.2 mmol/kg, orally), quercetin (0.2 mmol, orally) either alone or in combination, once daily for 5 consecutive days. Arsenic exposure led to a significant depletion of blood delta-aminolevulinic acid dehydratase (ALAD) activity, glutathione, white (WBC) and red blood cell (RBC) counts, and an increase in platelet levels while significantly increasing the level of reactive oxygen species (in RBCs). Hepatic reduced catalase (CAT) and glutathione peroxidase activities showed a depletion, whereas thiobarbituric acid reactive substances (TBARS) levels increased on arsenic exposure indicating arsenite-induced oxidative stress in blood and liver. Kidney CAT activity showed a depletion, whereas TBARS levels increased on arsenic exposure. These biochemical changes were accompanied by an increase in blood, liver, and kidney arsenic concentration. Treatment with MiADMSA was effective in increasing ALAD activity, whereas quercetin was ineffective when given alone. Quercetin when co-administered with MiADMSA also provided no additional beneficial effect on blood ALAD activity but significantly brought altered platelet counts nearer to the normal value. In contrast, administration of quercetin alone provided significant beneficial effects on hepatic oxidative stress and kidney TBARS levels. Renal biochemical variables remained insensitive to arsenic and any of the treatments. Interestingly, combined administration of quercetin with MiADMSA had a remarkable effect in depleting total arsenic concentration from blood and soft tissues. These results lead us to conclude that quercetin administration during chelation treatment had some beneficial effects particularly on the protection of inhibited blood ALAD activity and depletion of arsenic level from target organs. The study supports our earlier conclusion that a co-administration of an antioxidant particularly flavonoids more beneficial than monotherapy with the chelating agents to achieve optimal effects of chelation in arsenite toxicity.

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Section: Introductionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Quercetin Administration During Chelation Therapy Protects Arsenic-Induced Oxidative Stress in Mice

Mishra

Flora

2008

Biol Trace Elem Res

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“…Beneficial role of antioxidants have been reported earlier against arsenic toxicity using rat model (Nandi et al 2006). Basic information on arsenical poisoning in cattle and small ruminants are meagre, except a report of development of anemia, gastrointestinal signs, toxic nephropathy and mortality in goats with induced chronic arsenic toxicity (Biswas et al 1998).…”

mentioning

confidence: 99%

Effect of Vitamin E Supplementation on Arsenic Induced Oxidative Stress in Goats

Das

Mani

Kaur

et al. 2012

Bull Environ Contam Toxicol

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The present study was designed to assess whether supplementation of different levels of vitamin E to long-term arsenic exposed goats affords protection against the oxidative stress caused by the metalloid. Twenty-four crossbred lactating goats were distributed randomly into four groups (control, T(1), T(2) and T(3)) of six in each. The animals in T(1), T(2) and T(3) were given 50 mg/kg DM arsenic daily, while in T(2) and T(3), vitamin E @100 IU and 150 IU/kg DM, respectively, was also supplemented additionally for the period of 12 months. Compared to control, significant (p < 0.05) decline in SOD (45 %), CAT activities of erythrocytes (63 %), plasma total Ig (22 %) and total antioxidant activity (24 %) was observed in only arsenic treated groups and vitamin E supplementation in both doses produced partial mitigation effect against SOD (23 %, 20 %) and CAT (39 %, 48 %) while complete mitigation against total Ig (16 %, 7 %) and antioxidant activity (10 %, 8 %) was found. Average lymphocyte stimulation index at the end of experiment was (p < 0.05) lower in arsenic exposed groups (1.003 ± 0.01) and significant (p < 0.05) recovery was observed in response of vitamin E supplementation at higher doses (1.138 ± 0.03). So, vitamin E is helpful in reducing the burden of arsenic induced oxidative stress and activities of antioxidant enzymes in goats.

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“…AS is a known human carcinogen and causes various forms of malignancy and tumors of the skin, urinary bladder, liver, kidney and lung (Smith et al, 1992;Chen et al, 1992;Cui et al, 2006;Suzuki et al, 2008;Liu and Walkes, 2008). The health eff ects of toxic levels of AS are multidimensional in both human and animal populations (Nandi et al, 2006). Liver and kidneys are considered as the primary targets for its toxico-pathological manifestations, and there are reports of biochemical alterations indicative of hepatic and renal system involvement in AS toxicity in animals (Biswas et al, 1998;Santra et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Effectiveness of zinc in modulating perinatal effects of arsenic on the teratological effects in mice offspring

et al. 2013

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Exposure to arsenic via drinking water is considered as a worldwide problem. Studies have shown that arsenic exposure during pregnancy aff ects embryogenesis and off spring development in rats and mice. Zinc as a micronutrient regulates many physiological functions, including an antioxidative role under various toxic conditions. However, studies on the perinatal protective eff ect of zinc on off spring need further attention. The present study was designed to evaluate the potential protective role of zinc in mitigating the adverse eff ects in the off spring of arsenic exposure during pregnancy. The arsenic (40mg/kg body weight) and zinc (4% w/v) doses formed the only drinking fl uid source for the experimental groups of dams during the perinatal period of the experiment. The early development of sensory motor coordination refl exes together with morphological development in the male pups was measured during the weaning period. In adolescence, the off spring were tested for their motor behavior. The enzyme γ-glutamyl transferase (γ-GT) and the oxidative stress indices like reduced glutathione (GSH) and lipid peroxidation (TBARS) were also estimated in the serum of the young adult male mice. Perinatal arsenic exposure caused depletion in body weight gain, delay in morphological development and retardation in the development of all sensory motor refl exes of the pups. In young adults, signifi cant decrease in motor behavior with signifi cant decrease in GSH level in the serum was observed. On the other hand, γ-GT and TBARS were signifi cantly increased in the serum due to arsenic treatment. However, animals exposed to arsenic in the presence of zinc showed a remarkable ameliorating eff ect of zinc on all observed teratological and biochemical arsenic toxicity in male off spring. It was observed that zinc has an antioxidative role in the perinatal toxicity of arsenic. It is concluded from the present study that zinc consumed during the perinatal period of pregnancy can ameliorate the possible toxicities of arsenic exposure in the off spring by acting as an ameliorative supplement.

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Oxidative stress indices and plasma biochemical parameters during oral exposure to arsenic in rats

Cited by 87 publications

References 27 publications

Quercetin Administration During Chelation Therapy Protects Arsenic-Induced Oxidative Stress in Mice

Quercetin Administration During Chelation Therapy Protects Arsenic-Induced Oxidative Stress in Mice

Effect of Vitamin E Supplementation on Arsenic Induced Oxidative Stress in Goats

Effectiveness of zinc in modulating perinatal effects of arsenic on the teratological effects in mice offspring

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