Molecular and cellular biochemistry
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Mol. Cell. Biochem. · Feb 2012
Toxicity of octanoate and decanoate in rat peripheral tissues: evidence of bioenergetic dysfunction and oxidative damage induction in liver and skeletal muscle.
The accumulation of octanoic (OA) and decanoic (DA) acids in tissue is the common finding in medium-chain acyl-coenzyme A dehydrogenase deficiency (MCADD), the most frequent defect of fatty acid oxidation. Affected patients present hypoketotic hypoglycemia, rhabdomyolysis, hepatomegaly, seizures and lethargy, which may progress to coma and death. At present, the pathophysiological mechanisms underlying hepatic and skeletal muscle alterations in affected patients are poorly known. ⋯ Finally, DA, but not OA, significantly decreased GSH levels in rat skeletal muscle. Our present data show that the medium-chain fatty acids that accumulate in MCADD impair electron transfer through respiratory chain and elicit oxidative damage in rat liver and skeletal muscle. It may be therefore presumed that these mechanisms are involved in the pathophysiology of the hepatopathy and rhabdomyolysis presented by MCADD-affected patients.
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Mol. Cell. Biochem. · Feb 2012
The effect of sevoflurane on the expression of M1 acetylcholine receptor in the hippocampus and cognitive function of aged rats.
Our aim is to investigate the effect of 1.5 and 3.0% sevoflurane on the expression of M(1) acetylcholine receptor (mAChR M(1)) in the hippocampus and the cognitive function of aged rats. Forty Sprague-Dawley (SD) rats of 12-month old were randomly divided into five groups. All SD rats received 1.5 or 3.0% sevoflurane in a special glass anesthesia box for 2 h, respectively, except for the normal control group. ⋯ The results showed that 3% sevoflurane induced the decline of cognitive function and significantly decreased the mAChR M(1) expression at mRNA levels at 1 day in the 3.0% sevoflurane I group when compared with the normal control group. However, there was no significant difference among the other groups when compared with normal control group. Therefore, administration of sevoflurane might temporally affect the ability of cognitive function of rats through suppressing the mAChR M(1) expression at mRNA levels in hippocampus.