Mitochondrial enzyme

The precursor, 7-dehydrocholesterol is converted by a non-enzymatic reaction to cholecalciferol (calciol). This reaction occurs in skin exposed to sunlight due to irradiation by UV-B light at a wavelength of about 300 nm. Cholecalciferol is transported via carrier proteins to the liver where hydroxylation at carbon-25 occurs in a reaction catalysed by a microsomal cytochrome P450 hydroxylase to form calcidiol. This compound travels to the kidney attached to specific binding proteins, where another cytochrome P450 enzyme, mitochondrial 1-a-hydroxylase, introduces a second hydroxyl group in to the molecule to form the active calcitriol. 

Induction For example, antioxidant enzymes, mitochondrial, membrane hyperpolarization, mitochondrial biogenesis... 

As mentioned, the mildness of NaBHaCN (coupled with its effectiveness and stability in aqueous media) has attracted considerable interest for applications in biochemical areas. Examples include the trapping of suspected imine intermediates produced in enzyme (mitochondrial monoamine oxidase) inactivation by amines, the establishment by reduction of the positions of imine-forming amines in 2-keto-3-deoxy-6-phosphogluconate aldolase, and the transfer labeling of methionyl-tRNA synthetase and methionyl-tRNA transformalase by treatment with periodate-treated tRNA. In fact, most biochemical applications of NaBHaCN have utilized in situ imine formation-reduction (i.e. reductive amination) conditions and will be further discussed in Section 1.2.2.3.1. 

Physiological compensation. This category includes genes involved in adaptive biochemical pathways, such as HSPs, antioxidant enzymes, mitochondrial genes, lysosomal genes and metalloenzymes, for which toxic metals compete for binding in the active site. 

Institute, Lisbon, Portugal) in the August/September 2006 Townsend Letter for Doctors Patients. (Mitochondria are the subcellular organelles that produce cellular energy via the formation of ATP, or adenosine triphosphate.) The article speaks of breaks in the mitochondrial DNA (MTDNA) traceable to oxidative stress from free radicals and possibly to chemotherapy itself, which can lead to cellular defects, mutations, and cancer. The formation and renewal of MTDNA involves the enzyme mitochondrial polymerase (and the inhibition of this enzyme can be viewed as one more factor in this complex scenario). 

Liesivuori and Savolainen (1991) studied the biochemical mechanisms of toxicity of methanol and formic acid. Formic acid is an inhibitor of the enzyme mitochondrial cytochrome oxidase causing histotoxic hypoxia. It is, however, a weaker inhibitor than cyanide and hydrosulfide anions. The effects of its acidosis are dilation of cerebral vessels, facilitation of the entry of calcium ions into cells, loss of lysosomal latency, and deranged production of ATP, the latter affecting calcium reabsorption in the kidney tubules. Also, urinary acidification from formic acid and its excretion may cause continuous recycling of the acid by the tubular cell Cl-/formate exchanger. Such sequence of events probably causes an accumulation of formate in urine. Other than methanol, methyl ethers, esters, and amides also metabolize forming formic acid. 

REGULATION OF THE KETOGENIC ENZYME MITOCHONDRIAL 3-HYDROXY-3-METHYLGLUTARYL-COA SYNTHASE IN ASTROCYTES AND MENINGEAL FIBROBLASTS... 

Cullingford, T.E, Bhakoo, K.K. Clark, J.B. (1998) J. Neurochem. 71, 1804-1812. Hormonal regulation of the mRNA encoding the ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in neonatal primary cultures of cortical astrocytes and meningeal fibroblasts. 

Not all the cyanide that is absorbed by the body undergoes oxygen inhibition. It is known that 80% of the absorbed cyanide is detoxified in the liver by the enzyme mitochondrial rhodanase. The enzyme catalyzes the transfer of a sulfur atom to combine with the cyanide to form the less toxic thiocyanate, which is excreted in the urine. In high exposures to cyanide, the sulfur donors are rapidly depleted and cyanide metaboUsm is slowed (Pope and Rail, 1995). The half-life for the conversion of cyanide to thiocyanate from a nonlethal dose in humans is between 20 and 60 minutes (CHEM-BANK, 1999). 

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