Cobalamin inactivation by nitrous oxide produces severe neurological impairment in fruit bats : Protection by methionine and aggravation by folates
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Knowledge gaps in understanding the metabolic and clinical effects of excess folates/folic acid: A summary, and perspectives, from an NIH workshop
2020, American Journal of Clinical NutritionWhite matter changes in chronic alcoholic liver disease: Hypothesized association and putative biochemical mechanisms
2015, Medical HypothesesCitation Excerpt :Following up on this early evidence, several papers demonstrated that direct supplementation of the diet with methionine significantly delayed/lessened the development of neuropathy. Subsequent studies in the fruit bat [50] and in the pig [51] demonstrated equivalent findings of N2O-induced myelopathy resembling the effects of B12 deficiency. These studies also confirmed that methionine supplementation is significantly protective against the development of such myelopathy.
Nitrous oxide-induced B<inf>12</inf> deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B<inf>12</inf>
2011, Journal of the Neurological SciencesCitation Excerpt :The substance of many of these reports is to stress that this association exists. However, this fact is not novel, for example, to the clinical biochemist, since N2O exposure has been widely used in the past two decades as the most effective way to produce animal models of B12 deficiency [10–12]. Nonetheless, clinical cases, when encountered, provide the opportunity to review the complex biochemistry of vitamin B12, to address a variety of issues regarding the pathogenesis of the clinical syndromes of B12 deficiency, and to highlight some of the still unanswered questions regarding the precise mechanisms by which B12 deficiency leads to neurologic damage, and how this damage is potentiated by N2O exposure.
Vitamin B12, folic acid, and the nervous system
2006, Lancet NeurologyCitation Excerpt :The inverse correlation between anaemia and neurological disability in vitamin-B12 deficiency may reflect a more harmful effect of folic acid on the nervous system or greater masking effect on the blood. In fruit bats deficient of vitamin B12, pretreatment with folates speeds up the onset of nitrous-oxide induced SCD.134 The key to the metabolic understanding of both the neurology and haematology of vitamin-B12 and folate deficiency is the synthesis of methionine from homocysteine by methionine synthase in which both 5-methyl-tetrahydrofolate and vitamin B12 act as cofactors (figure 1).
Acute neurological disclorure of B12 avitaminosis induced by folic acid administration
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