Metabolism of Mycotoxins, Intracellular Functions of Vitamin B ₁₂, and Neurological Manifestations in Patients with Chronic Toxigenic Mold Exposures. A Review

Abstract

This paper evaluates the possible reasons for consistent vitamin B ₁₂ deficiency in chronic toxigenic mold exposures and the synergistic relationships with the possible mycotoxic effects on one-carbon metabolism that lead to the manifestations of clinical neuropathological symptomology. Vitamins are first defined in general and the nutritional sources of vitamin B ₁₂ are evaluated in particular. Since patients with chronic exposures to toxigenic molds manifest vitamin B ₁₂ deficiencies, the role of mycotoxins in vitamin B ₁₂ metabolism is assessed, and since vitamin B ₁₂ plays important biochemical roles in one-carbon metabolism, the synergistic effects with mycotoxins on humans are reviewed. An outline of the proposed mechanism by which mycotoxins disrupt or interfere with the normal functions of vitamin B ₁₂ on one-carbon metabolism is proposed. The overall functions of vitamin B ₁₂ as a source of coenzymes, in intracellular recycling of methionine, in methionine synthase reaction, in the prevention of chromosome breakage, in methylation, and in maintaining a one-carbon metabolic balance are reviewed. Signs, symptoms, and clinical neurological indications of vitamin B ₁₂ deficiency are also cited. By implication and derivation, it is likely that the interruption of the structure and function of vitamin B ₁₂ would in turn interfere with the one-carbon metabolism leading to the neurological manifestations. This review is an attempt to formulate a basis for an ongoing research investigation on the subject.