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Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice.
Toxicology 2008; 252(1-3):86-91T

Abstract

The protective effects of diallyl trisulfide (DATS) on acute ethanol-induced liver injury were investigated. Mice were pretreated with DATS (30mg/kgbw) for 7d before being exposed to ethanol (4.8g/kgbw). The biochemical indices (aspartate amino transferase, AST; alanine amino transferase, ALT; triglyceride, TG) were examined to evaluate the protective effects. Mitochondria were isolated for the mitochondrial permeability transition (MPT), membrane potential (DeltaPsi(m)) and adenosine nucleotide pool assay. The lipid peroxidation (malondialdehyde, MDA), non-enzymatic antioxidant (glutathione, GSH) and enzymatic antioxidants (superoxide dismutase, SOD; catalase, CAT; glutathione reductase, GR; glutathione peroxidase, GSH-Px) were measured both in the liver homogenate and isolated mitochondria. Acute ethanol exposure resulted in the significant increase of the ALT, AST and TG levels and hepatic mitochondria dysfunction shown as MPT, and the decreases of DeltaPsi(m), ATP and energy charge (EC). However, DATS pretreatment dramatically attenuated these adverse effects. Beside this, DATS was found to significantly inhibit the increase of the hepatic and mitochondrial MDA levels, which were decreased by 33.3% (P<0.01) and 39.0% (P<0.01), respectively. In addition, DATS pretreatment markedly suppressed the ethanol-induced decrease of the hepatic GSH level and increased the mitochondrial GSH level. Moreover, the activities of the hepatic antioxidant enzymes (SOD, CAT, and GR) and the mitochondrial antioxidant enzymes (SOD, GR, and GSH-Px) were significantly boosted. Thus, we concluded that DATS dramatically attenuated acute ethanol-induced liver injury and mitochondrial dysfunction. The increase of the hepatic and mitochondrial GSH levels and the elevation of the antioxidant enzymes activities should account for the preventive effects.

Authors+Show Affiliations

Institute of Toxicology, Shandong University, 44 Wenhua West Road, Shandong, Jinan 250012, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18755235

Citation

Zeng, Tao, et al. "Diallyl Trisulfide (DATS) Effectively Attenuated Oxidative Stress-mediated Liver Injury and Hepatic Mitochondrial Dysfunction in Acute Ethanol-exposed Mice." Toxicology, vol. 252, no. 1-3, 2008, pp. 86-91.
Zeng T, Zhang CL, Zhu ZP, et al. Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice. Toxicology. 2008;252(1-3):86-91.
Zeng, T., Zhang, C. L., Zhu, Z. P., Yu, L. H., Zhao, X. L., & Xie, K. Q. (2008). Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice. Toxicology, 252(1-3), pp. 86-91. doi:10.1016/j.tox.2008.07.062.
Zeng T, et al. Diallyl Trisulfide (DATS) Effectively Attenuated Oxidative Stress-mediated Liver Injury and Hepatic Mitochondrial Dysfunction in Acute Ethanol-exposed Mice. Toxicology. 2008 Oct 30;252(1-3):86-91. PubMed PMID: 18755235.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice. AU - Zeng,Tao, AU - Zhang,Cui-Li, AU - Zhu,Zhen-Ping, AU - Yu,Li-Hua, AU - Zhao,Xiu-Lan, AU - Xie,Ke-Qin, Y1 - 2008/08/07/ PY - 2008/06/26/received PY - 2008/07/29/revised PY - 2008/07/29/accepted PY - 2008/8/30/pubmed PY - 2009/1/6/medline PY - 2008/8/30/entrez SP - 86 EP - 91 JF - Toxicology JO - Toxicology VL - 252 IS - 1-3 N2 - The protective effects of diallyl trisulfide (DATS) on acute ethanol-induced liver injury were investigated. Mice were pretreated with DATS (30mg/kgbw) for 7d before being exposed to ethanol (4.8g/kgbw). The biochemical indices (aspartate amino transferase, AST; alanine amino transferase, ALT; triglyceride, TG) were examined to evaluate the protective effects. Mitochondria were isolated for the mitochondrial permeability transition (MPT), membrane potential (DeltaPsi(m)) and adenosine nucleotide pool assay. The lipid peroxidation (malondialdehyde, MDA), non-enzymatic antioxidant (glutathione, GSH) and enzymatic antioxidants (superoxide dismutase, SOD; catalase, CAT; glutathione reductase, GR; glutathione peroxidase, GSH-Px) were measured both in the liver homogenate and isolated mitochondria. Acute ethanol exposure resulted in the significant increase of the ALT, AST and TG levels and hepatic mitochondria dysfunction shown as MPT, and the decreases of DeltaPsi(m), ATP and energy charge (EC). However, DATS pretreatment dramatically attenuated these adverse effects. Beside this, DATS was found to significantly inhibit the increase of the hepatic and mitochondrial MDA levels, which were decreased by 33.3% (P<0.01) and 39.0% (P<0.01), respectively. In addition, DATS pretreatment markedly suppressed the ethanol-induced decrease of the hepatic GSH level and increased the mitochondrial GSH level. Moreover, the activities of the hepatic antioxidant enzymes (SOD, CAT, and GR) and the mitochondrial antioxidant enzymes (SOD, GR, and GSH-Px) were significantly boosted. Thus, we concluded that DATS dramatically attenuated acute ethanol-induced liver injury and mitochondrial dysfunction. The increase of the hepatic and mitochondrial GSH levels and the elevation of the antioxidant enzymes activities should account for the preventive effects. SN - 0300-483X UR - https://www.unboundmedicine.com/medline/citation/18755235/Diallyl_trisulfide__DATS__effectively_attenuated_oxidative_stress_mediated_liver_injury_and_hepatic_mitochondrial_dysfunction_in_acute_ethanol_exposed_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-483X(08)00370-3 DB - PRIME DP - Unbound Medicine ER -