Many biological subdisciplines that regularly assess dose–response relationships have
identified an evolutionarily conserved process in which a low dose of a stressful stimulus …

Tissue repair is a dynamic compensatory cell proliferation and tissue regeneration response
stimulated in order to overcome acute toxicity and recover organ/tissue structure and …

This review focuses on cellular events that modulate hepatotoxicity subsequent to initial
liver insult. Cellular events that determine the nature and extent of hepatotoxic injury and the …

Thioacetamide (TA), a potent centrilobular hepatotoxicant, undergoes a two-step bioactivation
mediated by microsomal CYP2E1 to TA sulfoxide (TASO), and further to TA-S,S-dioxide (…

Thioacetamide (TA)-induced hepatotoxicity is potentiated in streptozotocin (STZ)-induced
diabetic rats. The relative roles of CYP2E1 and FMO1 in the mechanism of TA-associated liver …

Earlier studies have shown highly exaggerated mechanism-based liver injury of thioacetamide
(TA) in rats following moderate diet restriction (DR) and in diabetes. The objective of the …

… Rao VC, Mehendale HM. Effect ofantimitotic agent colchicine on carbon tetrachloride toxicity…
Mehendale HM. Amplified interactive toxicity of chemicals at nontoxic levels: mechanistic …

The National Toxicology Program (NTP) and the National Institute of Environmental Health
Sciences (NIEHS) established the NTP Center for the Evaluation of Risks to Human …

CCl 4 is a hepatotoxic haloalkane, capable of producing hepatocellular fatty degeneration
and centrilobular necrosis. Previous reports indicate induction of liver regeneration after 36-…

Thioacetamide (TA) is bioactivated by CYP2E1 to TA sulfoxide (TASO), and to the highly
reactive sulfdioxide (TASO 2 ), which initiates hepatic necrosis by covalent binding. Previously, …