title: Diallyl trisulfide modulates cell viability and the antioxidation and detoxification systems of rat primary hepatocytes.
abstract: This study investigated the effects of various concentrations of diallyl trisulfide (DATS) and incubation times on cell viability, glutathione (GSH) content, and GSH-related enzyme activity in rat primary hepatocytes. Isolated and cultured primary rat hepatocytes were used as an experimental model. Cells were treated with 0 (control), 0.025, 0.05, or 0.25 mmol/L DATS for 0, 4, 8, or 24 h. After 24 h of treatment, some cells were incubated in fresh medium without DATS for an additional 24 h (48-h incubations). Based on lactate dehydrogenase (LDH) leakage and morphological examination, hepatocytes treated with 0.025 mmol/L DATS did not differ from the control cells at 4, 8, 24, and 48 h of incubation. However, LDH leakage was higher than in the control cells (P < 0.05) when the hepatocytes were treated with 0.05 or 0.25 mmol/L DATS for 4 h or more. The intracellular GSH levels of hepatocytes treated with 0.025 or 0.05 mmol/L DATS were higher than those of the control cells (P < 0.05), whereas those treated with 0.25 mmol/L DATS did not differ. The activity of glutathione reductase (GRd) was higher than in the control cells at 24 h (P < 0.05) when the hepatocytes were treated with 0.025 mmol/L DATS. When the hepatocytes were treated with 0.025 mmol/L DATS, the activity of glutathione S-transferase (GST) was higher than in the control cells at 48 h (P < 0.05). In hepatocytes treated with 0.05 mmol/L DATS, the activity of GST and glutathione peroxidase (GPx) was higher than in the control cells (P < 0.05) at 24 and 48 h of incubation. The results indicate that 0.025 or 0.05 mmol/L DATS could enhance antioxidation and detoxification capabilities by increasing the intracellular GSH level and the activity of GPx, GRd, or GST in rat primary hepatocytes. However, 0.05 or 0.25 mmol/L DATS might adversely affect the viability of hepatocytes.
authors.affiliation: Department of Nutrition and Health Science, Fooyin University, Kaohsiung, Taiwan.
authors.forename: Chih-Chung
authors.initials: CC
authors.lastname: Wu
authors.forename: Chong-Kuei
authors.initials: CK
authors.lastname: Lii
authors.forename: Shun-Jen
authors.initials: SJ
authors.lastname: Tsai
authors.forename: Lee-Yan
authors.initials: LY
authors.lastname: Sheen
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects*; D002478:Cells, Cultured; D005978:Glutathione / Q000032:analysis; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000032:analysis / Q000378:metabolism; D022781:Hepatocytes / Q000187:drug effects* / Q000502:physiology*; D008658:Inactivation, Metabolic; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides / Q000494:pharmacology*
chemical_list: D000498:Allyl Compounds; D000975:Antioxidants; D007527:Isoenzymes; D013440:Sulfides; C042577:diallyl trisulfide; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione