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Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats.
Hum Exp Toxicol 2015; 34(5):506-25HE

Abstract

The present study investigates the possible ameliorative effects of diallyl trisulfide (DATS) against arsenic (As)-induced hepatotoxicity and oxidative stress in rats. The four experimental groups evaluated include: (1) vehicle control; (2) As (5 mg/kg/day); (3) DATS (80 mg/kg/day) + As; and (4) DATS. Induction of As in rats caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities and increased total bilirubin concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in the liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione content, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and the significant increase in lipid peroxidation (thiobarbituric acid reactive substance) and protein oxidation (protein carbonyl) contents indicated that As-induced hepatotoxicity was mediated through oxidative stress. As intoxication also elevated the levels of Cas-3 and nitric oxide and increased the expression of nuclear factor-κB p65 in the liver. In contrast, DATS pretreatment significantly improved As-induced serum biochemical, immunohistochemical, and histopathological alterations reflecting hepatic dysfunction. These results may contribute to a better understanding of the hepatoprotective role of DATS, emphasizing the influence of this garlic trisulfide in the diet for human health, possibly preventing the hepatic injury associated with As intoxication, presumably due to its ability to inhibit lipid peroxidation, protein oxidation, and restoration of antioxidant status.

Authors+Show Affiliations

Department of Zoology, Annamalai University, Annamalainagar, Tamil Nadu, India.Department of Zoology, Annamalai University, Annamalainagar, Tamil Nadu, India smprabu73@gmail.com.

Pub Type(s)

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

Language

eng

PubMed ID

25062976

Citation

Sumedha, N C., and S Miltonprabu. "Diallyl Trisulfide Ameliorates Arsenic-induced Hepatotoxicity By Abrogation of Oxidative Stress, Inflammation, and Apoptosis in Rats." Human & Experimental Toxicology, vol. 34, no. 5, 2015, pp. 506-25.
Sumedha NC, Miltonprabu S. Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats. Hum Exp Toxicol. 2015;34(5):506-25.
Sumedha, N. C., & Miltonprabu, S. (2015). Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats. Human & Experimental Toxicology, 34(5), pp. 506-25. doi:10.1177/0960327114543933.
Sumedha NC, Miltonprabu S. Diallyl Trisulfide Ameliorates Arsenic-induced Hepatotoxicity By Abrogation of Oxidative Stress, Inflammation, and Apoptosis in Rats. Hum Exp Toxicol. 2015;34(5):506-25. PubMed PMID: 25062976.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats. AU - Sumedha,N C, AU - Miltonprabu,S, Y1 - 2014/07/25/ PY - 2014/7/27/entrez PY - 2014/7/27/pubmed PY - 2016/1/12/medline KW - Arsenic KW - antioxidant KW - diallyl trisulfide KW - hepatotoxicity KW - liver KW - oxidative stress SP - 506 EP - 25 JF - Human & experimental toxicology JO - Hum Exp Toxicol VL - 34 IS - 5 N2 - The present study investigates the possible ameliorative effects of diallyl trisulfide (DATS) against arsenic (As)-induced hepatotoxicity and oxidative stress in rats. The four experimental groups evaluated include: (1) vehicle control; (2) As (5 mg/kg/day); (3) DATS (80 mg/kg/day) + As; and (4) DATS. Induction of As in rats caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities and increased total bilirubin concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in the liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione content, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and the significant increase in lipid peroxidation (thiobarbituric acid reactive substance) and protein oxidation (protein carbonyl) contents indicated that As-induced hepatotoxicity was mediated through oxidative stress. As intoxication also elevated the levels of Cas-3 and nitric oxide and increased the expression of nuclear factor-κB p65 in the liver. In contrast, DATS pretreatment significantly improved As-induced serum biochemical, immunohistochemical, and histopathological alterations reflecting hepatic dysfunction. These results may contribute to a better understanding of the hepatoprotective role of DATS, emphasizing the influence of this garlic trisulfide in the diet for human health, possibly preventing the hepatic injury associated with As intoxication, presumably due to its ability to inhibit lipid peroxidation, protein oxidation, and restoration of antioxidant status. SN - 1477-0903 UR - https://www.unboundmedicine.com/medline/citation/25062976/Diallyl_trisulfide_ameliorates_arsenic_induced_hepatotoxicity_by_abrogation_of_oxidative_stress_inflammation_and_apoptosis_in_rats_ L2 - http://journals.sagepub.com/doi/full/10.1177/0960327114543933?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -