Inhibition of cocaine oxidative metabolism attenuates endotoxin potentiation of cocaine mediated hepatotoxicity.

The oxidative metabolism of cocaine by the microsomal monooxygenase enzymes has been postulated to be essential for cocaine mediated hepatotoxicity (CMH). Endotoxin (lipopolysaccharide, LPS), a well-known cause of hepatic damage, previously has been demonstrated to dramatically increase CMH. The mechanism of this interaction has not been clearly elucidated, but cocaine oxidative metabolism appears to sensitize hepatocytes so that subsequent exposure to small amounts of LPS can further augment CMH.

Endotoxin potentiates the hepatotoxicity of cocaine in male mice.

Cocaine produces hepatotoxicity by a mechanism that remains undefined but that has been linked to its oxidative metabolism. Endotoxin (lipopolysaccharide, LPS) is also a well-known cause of hepatic damage, where exposure to non-injurious doses of LPS increases the toxicity of certain hepatotoxins. This study was conducted to investigate the possible potentiation of cocaine-mediated hepatotoxicity (CMH) by LPS.

Development and validation of a high-performance liquid chromatography method for the determination of cocaine, its metabolites and ketamine.

Cocaine abuse is an extensive problem in the USA. During the past decade, ketamine abuse also has emerged as a public health concern and is now considered a controlled substance. The prevalence of the simultaneous use of cocaine and ketamine has been shown to be high.

The role of ketamine on plasma cocaine pharmacokinetics in rat.

Ketamine has gained attention recently because of re-emergence of its abuse especially in combination with cocaine. When more than one drug is present simultaneously, the potential for drug--drug interaction exists, which can be pharmacokinetic, pharmacodynamic or both in nature. The objective of this study was to investigate the effect of ketamine on plasma cocaine pharmacokinetics to assess the role that the kinetic component may play in the interaction of these agents.

In vitro hepatotoxicity of alachlor and its by-products.

During water treatment, potentially hazardous chemical by-products may be formed. Alachlor (2-chloro-N-(2, 6-diethylphenyl)-N-(methoxymethyl) acetamide) is a widely used pre-emergence herbicide. The present study investigated the toxicity of alachlor and its disinfection by-products on freshly isolated rat hepatocytes.