title: Comparative evaluation of the effects of taurine and thiotaurine on alterations of the cellular redox status and activities of antioxidant and glutathione-related enzymes by acetaminophen in the rat.
abstract: The present study was carried out to ascertain the impact of replacing the sulfonate group of TAU with thiosulfonate, as present in thiotaurine (TTAU), on the protective actions of TAU against hepatocellular damage and biochemical alterations related to oxidative stress and glutathione redox cycling, synthesis, and utilization caused by a high dose of acetaminophen (APAP). To this end, male Sprague-Dawley rats, 225-250 g, were intraperitoneally treated with a 2.4 mmol/kg dose of TAU (or TTAU), followed 30 min later by 800 mg/kg of APAP. A reference group received 2.4 mmol/kg of N-acetylcysteine (NAC) prior to APAP. Naive rats served as controls. The animals were sacrificed 6 h after receiving APAP and their blood and livers were collected. Plasma and liver homogenates were analyzed for indices of cell damage (plasma transaminases, plasma lactate dehydrogenase), -oxidative stress (malondialdehyde = MDA, reduced glutathione = GSH, glutathione disulfide = GSSG, catalase, glutathione peroxidase, superoxide dismutase), glutathione cycling (glutathione reductase), utilization (glutathione S-transferase), and synthesis (γ-glutamylcysteine synthetase) activities. APAP increased MDA formation and lowered the GSH/GSSG ratio and all enzyme activities, especially those of antioxidant enzymes. In general, TTAU was equipotent with NAC and more potent than TAU in protecting the liver. Taken into account the results of a previous study comparing the actions of TAU and hypotaurine (HTAU), the sulfinate analog of TAU, it appears that the sulfinate and thiosulfonate analogs are somewhat more effective than the parent sulfonate TAU in counteracting APAP-induced hepatic alterations in the liver and plasma.
authors: Department of Pharmaceutical Sciences, St. John's University, Jamaica, NY, USA.
authors: Miteshkumar
authors: M
authors: Acharya
authors: Cesar A
authors: CA
authors: Lau-Cam
mesh_terms: D000082:Acetaminophen / Q000009:adverse effects*; D000111:Acetylcysteine / Q000494:pharmacology; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001219:Aspartate Aminotransferases / Q000097:blood; D002374:Catalase / Q000097:blood; D005721:Glutamate-Cysteine Ligase / Q000097:blood; D005978:Glutathione / Q000097:blood / Q000378:metabolism*; D019803:Glutathione Disulfide / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D005982:Glutathione Transferase / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D010084:Oxidation-Reduction / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000097:blood; D013654:Taurine / Q000031:analogs & derivatives* / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D013654:Taurine; D000082:Acetaminophen; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005721:Glutamate-Cysteine Ligase; D005978:Glutathione; C514237:thiotaurine; D019803:Glutathione Disulfide; D000111:Acetylcysteine