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Biotransformation and cytotoxic effects of hydroxychavicol, an intermediate of safrole metabolism, in isolated rat hepatocytes.
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Metabolism and cytotoxicity of propyl gallate in isolated rat hepatocytes: effects of a thiol reductant and an esterase inhibitor.
TLDR
The results indicate that PG-induced hepatotoxicity is mediated by the parent compound and not its metabolites, that toxicity is associated with ATP depletion apparently independently of cellular thiol depletion, and that mitochondria may represent critical targets of PG- induced cytotoxicity.
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Presence of 2-amino-3,8-dimethylimidazo [4,5-f]quinoxaline (MeIQx) in dialysate from patients with uremia.
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Effects of N-acetyl-l-cysteine on target sites of hydroxylated fullerene-induced cytotoxicity in isolated rat hepatocytes
TLDR
Pretreatment with NAC ameliorates mitochondrial dysfunction linked to the depletion of ATP, MMP, and mitochondrial GSH level and induction of oxidative stress assessed by reactive oxygen species generation, losses of intracellular GSH and protein thiol levels, and MDA formation caused by C60(OH)24, suggesting that the onset of toxic effects is at least partially attributable to a thiol redox-state imbalance.
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Chlorpropham induces mitochondrial dysfunction in rat hepatocytes.
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On the mechanisms of 3-tert-butyl-4-hydroxyanisole- and its metabolites-induced cytotoxicities in isolated rat hepatocytes.
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[Toxicity assessments of chemical substances using primary culture of rat hepatocytes].
TLDR
The degree of toxicity in these chemicals seems to be almost identical to the degree of in vivo hepatotoxicity reported previously, and there is a positive correlation between PT50 calculated by the LD50 value reported previously and -Log magnitude of TCL0.
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Biotransformation of chlorpropham (CIPC) in isolated rat hepatocytes and xenoestrogenic activity of CIPC and its metabolites by in vitro assays
TLDR
The results suggest that even if CIPC is metabolized to 4OH-CIPC by hepatocytes, the chlorine adjacent to the 4-hydroxy group added to the intermediate as well as 3-chloro-butylparaben obstructs the appearance of oestrogen-like effects via an interaction between the intermediate and the ER.
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[Effects of tricyclohexyltin hydroxide on carbohydrate and lipid metabolisms].
TLDR
It is suggested that TCHT induces hyperglycemia and hyperlipidemia in rabbits, and the disturbance of metabolism seems to be related to the inhibition of insulin release from the pancreatic islets by T CHT.
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