Abstract
Carnosine (beta-alanyl-L-histidine), which is present in millimolar concentrations in skeletal muscles, induces Ca2+ release from the heavy fraction of rabbit skeletal muscle sarcoplasmic reticulum by activation ruthenium red-sensitive Ca-release channels. The effect of carnosine is dose-dependent, which indicates the presence of saturable carnosine-binding sites in the Ca-release channel molecule. The half-maximal Ca2+ release is observed in the presence of 8.7 mM carnosine. At the same time, carnosine addition to the medium increases the affinity of sarcoplasmic reticulum Ca-channels for the Ca-release activators, caffeine and adenine nucleotides. It is concluded that carnosine is an endogenous regulator of skeletal muscle sarcoplasmic reticulum Ca-channels which modulates the affinity of these channels for different ligands.
Highlights
Formaldehyde, the simplest aldehyde, is an environmental pollutant and human toxin
Formaldehyde detoxification involves its reaction with nucleophilic thiols: in plants, animals, and some bacteria, formaldehyde reacts with glutathione to give S-hydroxymethylglutathione, which is the substrate for an NAD-dependent dehydrogenase (e.g. ADH5 in humans)
The observations suggest that elevated levels of endogenous formaldehyde lead to DNA damage, which is not tolerated in Fanconi anemia (FA) repair-deficient cells
Summary
Formaldehyde, the simplest aldehyde, is an environmental pollutant and human toxin. Acute exposure to exogenous formaldehyde can cause irritation, nausea, renal failure, and coma. The research demonstrates that a functional glutathione-dependent formaldehyde metabolism pathway is required for survival of FA models.[3] The observations suggest that elevated levels of endogenous formaldehyde lead to DNA damage, which is not tolerated in FA repair-deficient cells.
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