Hepatic Damage Caused by Chronic Arsenic Toxicity in Experimental Animals

Santra, Amal; Maiti, A; Das, Saurabh; Lahiri, Sarbari; Charkaborty, Sushil K.; Mazumder, D. N. Guha; Mazumder, Debendra Guha

doi:10.1081/clt-100100949

Cited by 160 publications

(123 citation statements)

References 35 publications

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“…The results revealed the aberrant expression of genes encoding oxidative stress, DNA damage and repair, and cell proliferation (26). These findings are consistent with those observed in livers of animals chronically fed arsenic-containing water for 48 weeks and longer (27,28), and in livers of mice receiving repeated arsenic injections (28,29). These lesions and aberrant gene expressions could potentially progress to neoplastic changes as seen in chronic arsenic-transformed rat liver cells (30) as well as in mice given repeated arsenic injections where hepatic proliferative and pre-neoplastic lesions have recently been observed (29).…”

Section: Clinical Symptoms Of Patientssupporting

confidence: 80%

Chronic arsenic poisoning from burning high-arsenic-containing coal in Guizhou, China.

Liu

Zheng

Aposhian

et al. 2002

Environ Health Perspect

226

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Arsenic is an environmental hazard and the reduction of drinking water arsenic levels is under consideration. People are exposed to arsenic not only through drinking water but also through arsenic-contaminated air and food. Here we report the health effects of arsenic exposure from burning high arsenic-containing coal in Guizhou, China. Coal in this region has undergone mineralization and thus produces high concentrations of arsenic. Coal is burned inside the home in open pits for daily cooking and crop drying, producing a high concentration of arsenic in indoor air. Arsenic in the air coats and permeates food being dried producing high concentrations in food; however, arsenic concentrations in the drinking water are in the normal range. The estimated sources of total arsenic exposure in this area are from arsenic-contaminated food (50-80%), air (10-20%), water (1-5%), and direct contact in coal-mining workers (1%). At least 3,000 patients with arsenic poisoning were found in the Southwest Prefecture of Guizhou, and approximately 200,000 people are at risk for such overexposures. Skin lesions are common, including keratosis of the hands and feet, pigmentation on the trunk, skin ulceration, and skin cancers. Toxicities to internal organs, including lung dysfunction, neuropathy, and nephrotoxicity, are clinically evident. The prevalence of hepatomegaly was 20%, and cirrhosis, ascites, and liver cancer are the most serious outcomes of arsenic poisoning. The Chinese government and international organizations are attempting to improve the house conditions and the coal source, and thereby protect human health in this area.

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Section: Clinical Symptoms Of Patientssupporting

confidence: 80%

Chronic arsenic poisoning from burning high-arsenic-containing coal in Guizhou, China.

Liu

Zheng

Aposhian

et al. 2002

Environ Health Perspect

226

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“…31,32 Therefore, we asked whether trolox could affect As 2 O 3 -associated hepatocellular damage in vivo. Mice were randomly divided into groups of five mice and treated with two doses of trolox and a dose of As 2 O 3 (7.5 mg/kg) reported to be moderately toxic.…”

Section: Trolox Significantly Enhances As 2 O 3 -Induced Apoptosis Ofmentioning

confidence: 99%

Trolox enhances the anti-lymphoma effects of arsenic trioxide, while protecting against liver toxicity

et al. 2007

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Arsenic trioxide (As 2 O 3 ) is an effective therapy in acute promyelocytic leukemia (APL), but its use in other malignancies is limited by the higher concentrations required to induce apoptosis. We have reported that trolox, an analogue of a-tocopherol, increases As 2 O 3 -mediated apoptosis in a variety of APL, myeloma and breast cancer cell lines, while nonmalignant cells may be protected. In the present study, we extended previous results to show that trolox increases As 2 O 3 -mediated apoptosis in the P388 lymphoma cell line in vitro, as evidenced by decrease of mitochondrial membrane potential and release of cytochrome c. We then sought to determine whether this combination can enhance antitumor effects while protecting normal cells in vivo. In BDF 1 mice, trolox treatment decreased As 2 O 3 -induced hepatomegaly, markers of oxidative stress and hepatocellular damage. In P388 tumor-bearing mice, As 2 O 3 treatment prolonged survival, and the addition of trolox provided a further significant increase in lifespan. In addition, the combination of As 2 O 3 and trolox inhibited metastatic spread, and protected the tumor-bearing mice from As 2 O 3 liver toxicity. Our results suggest, for the first time, that trolox might prevent some of the clinical manifestations of As 2 O 3 -related toxicity while increasing its pro-apoptotic capacity and clinical efficacy in hematological malignancies.

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“…Thus an agent able to reduce the toxic potential of arsenic in liver cell would clearly be a use full compound for arsenical chemotherapy. The liver has long been identified as a target organ of arsenic exposure [27], its importance as an organ arsenic biotransformation is well established [28]. The mechanism by which arsenic directly damages the liver including oxidative stress [29,30], enhanced inflammation and alteration in cellular methylation status has been investigated [31].…”

Section: Discussionmentioning

confidence: 99%

Arsenic-Induced Hepatic Toxicity and Its Attenuation by Fruit Extract of Emblica officinalis (Amla) in Mice

et al. 2013

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Arsenic a metalloid and environmental contaminated has been found to be associated with public health problems in the affected areas. It is naturally occurred in groundwater and its accumulation in plant and animals leads to toxicity in several tissues most notably hepatic organ. Arsenic exposures (3 mg/kg body weight/ day for 30 days) in mice exhibited increased arsenic and Zn levels in hepatocytes associated with enhanced oxidative stress in hepatocytes while there were no significantly changes were observed in Cu level. An increase in the lipid peroxidation and decrease in the levels of reduced glutathione and activity of superoxide dismutase, catalase, and glutathione peroxidase were observed in arsenic treated mice as compared to controls. Arsenic exposure in mice also caused a significant change in serum biomarkers in the SGOT, SGPT and creatinine as compared to the controls. There were no significant changes in the serum levels of total protein in these mice. Co-administration of arsenic and fruit extract of amla (500 mg/kg body weight/day for 30 days) caused a significant reduction of arsenic transference associated with significantly decreases hepatic arsenic levels and balanced the antioxidant enzyme and levels of serum hepatic enzymes like SGOT and SGPT. The results of the present study clearly demonstrate the antioxidant property of amla that could be responsible for its protective efficacy in arsenic induced hepatic toxicity.

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Hepatic Damage Caused by Chronic Arsenic Toxicity in Experimental Animals

Cited by 160 publications

References 35 publications

Chronic arsenic poisoning from burning high-arsenic-containing coal in Guizhou, China.

Chronic arsenic poisoning from burning high-arsenic-containing coal in Guizhou, China.

Trolox enhances the anti-lymphoma effects of arsenic trioxide, while protecting against liver toxicity

Arsenic-Induced Hepatic Toxicity and Its Attenuation by Fruit Extract of Emblica officinalis (Amla) in Mice

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