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Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide.
Toxicol Mech Methods. 2014 Feb; 24(2):124-35.TM

Abstract

The present investigation was aimed to investigate the possible protective role of diallyl trisulfide (DATS) against arsenic (As)-induced hepatic mitochondrial toxicity in rats. Mitochondria were isolated from the liver tissue of rats from all the groups. Lipid profile, lipid peroxidation, antioxidant enzyme activities, hepatic function enzymes, mitochondrial swelling, cytochrome c oxidase activity, mitochondrial Ca(+)-ATPase and Na(+)/K(+)-ATPase activity, mitochondrial calcium content and mitochondrial enzyme activities were measured. Short-term As exposure (5 mg/kg bw/d for 28 d) caused liver damage as evidenced by changes in activities of liver enzymes. The effects of As were coupled with enhanced reactive oxygen species generation, mitochondrial swelling, inhibition of cytochrome c oxidase, complex I-mediated electron transfer, decreased Ca(2+)-ATPase and Na(+)/K(+)-ATPase activity, a reduction in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress, significant increase in mitochondrial lipid peroxidation products and alterations in mitochondrial lipid profile. Significant decreases in mitochondrial antioxidants and tricarboxylic acid cycle enzymes were also found in the liver mitochondria of As-induced hepatic mitochondrial toxicity in rats. As also increased hepatic caspase-3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by As could be alleviated by supplementation with DATS, which likely suggests a protective role against As-induced hepatotoxic changes and hepatic mitochondrial toxicity. The protective effect of DATS on the liver mitochondria was evidenced by altering all the changes induced by As. Free radical scavenging and metal chelating activities of DATS may be the mechanism, responsible for the protective action against As-induced mitochondrial damage in liver.

Authors+Show Affiliations

Department of Zoology, Faculty of Science, Annamalai University , Annamalainagar, Tamilnadu , India.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24295472

Citation

Miltonprabu, S, and N C. Sumedha. "Arsenic-induced Hepatic Mitochondrial Toxicity in Rats and Its Amelioration By Diallyl Trisulfide." Toxicology Mechanisms and Methods, vol. 24, no. 2, 2014, pp. 124-35.
Miltonprabu S, Sumedha NC. Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide. Toxicol Mech Methods. 2014;24(2):124-35.
Miltonprabu, S., & Sumedha, N. C. (2014). Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide. Toxicology Mechanisms and Methods, 24(2), 124-35. https://doi.org/10.3109/15376516.2013.869778
Miltonprabu S, Sumedha NC. Arsenic-induced Hepatic Mitochondrial Toxicity in Rats and Its Amelioration By Diallyl Trisulfide. Toxicol Mech Methods. 2014;24(2):124-35. PubMed PMID: 24295472.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide. AU - Miltonprabu,S, AU - Sumedha,N C, PY - 2013/12/4/entrez PY - 2013/12/4/pubmed PY - 2014/9/26/medline SP - 124 EP - 35 JF - Toxicology mechanisms and methods JO - Toxicol Mech Methods VL - 24 IS - 2 N2 - The present investigation was aimed to investigate the possible protective role of diallyl trisulfide (DATS) against arsenic (As)-induced hepatic mitochondrial toxicity in rats. Mitochondria were isolated from the liver tissue of rats from all the groups. Lipid profile, lipid peroxidation, antioxidant enzyme activities, hepatic function enzymes, mitochondrial swelling, cytochrome c oxidase activity, mitochondrial Ca(+)-ATPase and Na(+)/K(+)-ATPase activity, mitochondrial calcium content and mitochondrial enzyme activities were measured. Short-term As exposure (5 mg/kg bw/d for 28 d) caused liver damage as evidenced by changes in activities of liver enzymes. The effects of As were coupled with enhanced reactive oxygen species generation, mitochondrial swelling, inhibition of cytochrome c oxidase, complex I-mediated electron transfer, decreased Ca(2+)-ATPase and Na(+)/K(+)-ATPase activity, a reduction in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress, significant increase in mitochondrial lipid peroxidation products and alterations in mitochondrial lipid profile. Significant decreases in mitochondrial antioxidants and tricarboxylic acid cycle enzymes were also found in the liver mitochondria of As-induced hepatic mitochondrial toxicity in rats. As also increased hepatic caspase-3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by As could be alleviated by supplementation with DATS, which likely suggests a protective role against As-induced hepatotoxic changes and hepatic mitochondrial toxicity. The protective effect of DATS on the liver mitochondria was evidenced by altering all the changes induced by As. Free radical scavenging and metal chelating activities of DATS may be the mechanism, responsible for the protective action against As-induced mitochondrial damage in liver. SN - 1537-6524 UR - https://www.unboundmedicine.com/medline/citation/24295472/Arsenic_induced_hepatic_mitochondrial_toxicity_in_rats_and_its_amelioration_by_diallyl_trisulfide_ L2 - https://www.tandfonline.com/doi/full/10.3109/15376516.2013.869778 DB - PRIME DP - Unbound Medicine ER -