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Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial
Tao Zeng1, Cui-Li Zhang, Zhen-Ping Zhu
1Institute of Toxicology, Shandong University, 44 Wenhua West Road, Shandong, Jinan 250012, PR China.
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.
Insights
Diallyl trisulfide (DATS) protects against acute ethanol-induced liver injury by reducing oxidative stress and improving mitochondrial function. DATS pretreatment significantly attenuated liver damage and restored antioxidant enzyme activities.
Area of Science:
- Hepatology
- Toxicology
- Mitochondrial Biology
- Nutritional Biochemistry
Background:
- Acute ethanol consumption is a major cause of liver injury.
- Ethanol-induced liver damage involves oxidative stress and mitochondrial dysfunction.
- Diallyl trisulfide (DATS) is a compound with potential therapeutic properties.
Purpose of the Study:
- To investigate the protective effects of diallyl trisulfide (DATS) against acute ethanol-induced liver injury in mice.
- To elucidate the mechanisms underlying DATS's protective effects, focusing on oxidative stress and mitochondrial function.
Main Methods:
- Mice were pretreated with DATS before acute ethanol exposure.
- Biochemical markers of liver injury (AST, ALT, TG) were assessed.
- Mitochondrial function (MPT, DeltaPsi(m), ATP, EC) and oxidative stress markers (MDA, GSH, antioxidant enzymes) were measured.
Main Results:
- Ethanol exposure significantly increased liver injury markers and mitochondrial dysfunction.
- DATS pretreatment attenuated liver damage, reduced lipid peroxidation (MDA), and preserved mitochondrial function.
- DATS increased glutathione (GSH) levels and boosted the activities of hepatic and mitochondrial antioxidant enzymes (SOD, CAT, GR, GSH-Px).
Conclusions:
- Diallyl trisulfide (DATS) demonstrates significant protective effects against acute ethanol-induced liver injury.
- DATS mitigates liver damage by enhancing antioxidant defense mechanisms and maintaining mitochondrial integrity.
- The findings suggest DATS as a potential therapeutic agent for alcoholic liver disease.