Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxicity of ozone is solely due to its action as an oxidant. It is an extremely reactive gas which rapidly forms intermediate oxidizing derivatives after inhalation. High concentrations cause death from pulmonary oedema. Both pulmonary and extrapulmonary toxicity have been observed at lower concentrations of ozone, including those currently present in urban air. Pulmonary cellular and subcellular membranes appear to be particularly susceptible. A primary mechanism of this effect is the oxidative decomposition of polyunsaturated fatty acids, which has been demonstrated in rodent lungs after inhalation of ozone. Supporting evidence includes the potentiation of ozone toxicity by vitamin E deficiency and an increased use of this antioxidant vitamin during repetitive exposure to ozone. Other membrane effects include oxidation of thiol groups and, perhaps, of tryptophan. Microsomal alterations include a loss of lung cytochrome P450 which may also be related to lipid peroxidation. Extrapulmonary toxicity is not directly due to ozone but may represent in effect due to lipid peroxide decomposition products, particularly malonaldehyde. This three-carbon dialdehyde has been shown to alter cell membrane fluidity and to have mutagenic properties; the latter perhaps due to cross-linkage of DNA to histone.
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PMID:The pulmonary and extrapulmonary effects of ozone. 25 63

Vitamin E deficiency induces neuronal dysfunction and while oxidative stress is likely to be involved in mediating this process, the detailed mechanisms remain to be elucidated. Previously, we found axonal degeneration in the hippocampal CA1 region in vitamin E-deficient mice of 6 months of age (long-term). However, 3 month-old (short-term) vitamin E-deficient mice did not exhibit axonal degeneration in same region. In order to characterize the mechanisms involved in axonal degeneration in long-term vitamin E-deficient mice, we examined changes in microtubule-related proteins. Long-term vitamin E-deficiency led to significantly increased expression of the phosphorylated form of collapsin response mediator protein (CRMP)-2 compared to short-term deficiency. It is well known that CRMP-2 plays a crucial role in the maintenance of neurite function. Similarly, long-term vitamin E-deficiency significantly decreased the expression of silent mating type information regulation (SIRT)-2 mRNA compared to short-term deficiency. SIRT-2 belongs to a family of class III histone deacetylases (HDACs) and functions in the deacetylation of tubulins. Furthermore, the expression of microtubule-associated protein light chain (MAP-LC)3-2, which is a key autophagy protein was significantly higher in the short-term vitamin E-deficiency than the long-term deficiency. These results indicate that the mechanisms of axonal injury in long-term vitamin E-deficient mice are related to dysfunction in microtubules assembly via alterations in microtubule-related proteins and autophagy.
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PMID:Changes in microtubule-related proteins and autophagy in long-term vitamin E-deficient mice. 2456 62