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Mechanisms of hepatotoxicity.
TLDR
This review addresses recent advances in specific mechanisms of hepatotoxicity, including inducible nitric oxide synthase knockout mice, where nitration is prevented, but unscavenged superoxide production then causes toxic lipid peroxidation to occur instead. Expand
Inhibition of mitochondrial beta-oxidation as a mechanism of hepatotoxicity.
TLDR
Drugs and some endogenous compounds can sequester coenzyme A and/or inhibit mitochondrial beta-oxidation enzymes, and decrease mitochondrial DNA replication (dideoxynucleoside analogues), while other compounds act through a combination of different mechanisms. Expand
Mitochondrial dysfunction in NASH: causes, consequences and possible means to prevent it.
TLDR
There is accumulating evidence that mitochondrial dysfunction (more particularly respiratory chain deficiency) plays a key role in the physiopathology of NASH whatever its initial cause and that several drugs can prevent or even reverse NASH. Expand
NASH: a mitochondrial disease.
TLDR
The purpose of this review is to discuss the evidence, mechanisms and implications of mitochondrial dysfunction at the successive steps leading to NASH, as already partially reviewed elsewhere. Expand
The Ala16Val genetic dimorphism modulates the import of human manganese superoxide dismutase into rat liver mitochondria.
TLDR
Results show that the Ala-MnSOD/MTS allows efficient MnSOD import into the mitochondrial matrix, while the Val-variant causes partial arrest of the precursor within the inner membrane and decreased formation of the active MnS OD tetramer in the mitochondrial Matrix. Expand
Mitochondria in steatohepatitis.
TLDR
In patients with steatosis, mitochondrial ROS may oxidize hepatic fat deposits, as suggested in animal models, and lipid peroxidation products impair the flow of electrons along the respiratory chain, which may cause overreduction of respiratory chain components, further increasing mitochondrial ROS formation and lipidPeroxidation. Expand
Drug‐induced liver injury through mitochondrial dysfunction: mechanisms and detection during preclinical safety studies
TLDR
In vitro and in vivo investigations can be performed to determine if newly developed drugs disturb mitochondrial fatty acid oxidation and the oxidative phosphorylation process, deplete hepatic mitochondrial DNA, or trigger the opening of the mitochondrial permeability transition (MPT) pore, as drugs can be deleterious for hepatic mitochondria in some individuals but not in others. Expand
Hepatitis C virus core protein inhibits microsomal triglyceride transfer protein activity and very low density lipoprotein secretion: a model of viral‐related steatosis
TLDR
A new patho‐physiological animal model is proposed for induction of viral‐related steatosis whereby the core protein of HCV targets microsomal triglyceride transfer protein activity and modifies hepatic VLDL assembly and secretion. Expand
Nonalcoholic steatosis and steatohepatitis. V. Mitochondrial dysfunction in steatohepatitis.
TLDR
Rich diet and lack of exercise are causing a surge in the prevalence of obesity and hepatic steatosis, which causes "primary" steatohepatitis in some patients, which could cause more lipid peroxidation, cytokine induction, and fibrogenesis than in primary steato hepatitis. Expand
The ins and outs of mitochondrial dysfunction in NASH.
TLDR
Reducing the incidence of NASH will be a major challenge for hepatologists for the next decade because some genetic polymorphisms can significantly increase the risk of steatohepatitis and that several drugs can prevent or even reverse NASH. Expand
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