PubMed · 15440307
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J GERLOFF. 1950. [Biotin].. https://pubmed.ncbi.nlm.nih.gov/15440307/
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The vitamin folate is vital for all living creatures. Scientists have suggested that ultraviolet degradation of folate in vivo played a role in the evolution of mankind. In order to better understand the photodegradation of folate, we have provided a spectroscopic study of the ultraviolet photodegradation of aqueous folic acid under aerobic conditions. We found strong indications that the folic acid molecule is cleaved into p-aminobenzoyl-L-glutamic acid and 6-formyl pterin when exposed to ultraviolet radiation. When the irradiation continues, 6-formyl pterin is degraded to pterin-6-carboxylic acid. The photodegradation of folic acid is divided into three phases. In the first phase, the formation of photoproducts follows a zero order rate law. In the second phase the presence of photoproducts sensitizes the degradation of folic acid and the degradation process is accelerated. In the third phase the degradation of 6-formyl pterin to pterin-6-carboxylic acid is the dominating process. This reaction follows a first order rate law. We show that both 6-formyl pterin and pterin-6-carboxylic acid sensitize the photodegradation of folic acid. However, experiments performed in heavy water indicate that generation of singlet oxygen is probably not the explanation for the photosensitizing of folic acid.
A vast amount of case reports, open studies and, to a lesser extent, case-control studies have been published on the topic of psychopathology and folate deficiency. These studies reported a high incidence of serum folate deficiency in patients with various psychiatric disorders. Folate deficiency seems to be a particular consistent finding in depressive patients. The evidence for an association between aberrant folate status and schizophrenia seems less convincing. The lack of stringent methodology such as inclusion of age- and sex-matched controls was thought to be the main reason for the inconclusive results. The purpose of this article is to review the published case-control studies that provide data on folate levels in the population of patients with schizophrenia. Data extracted from these studies comprised methodological design, clinical characteristics and folate measurements. We found that none of the 7 case-control studies included in this review (in total 325 cases and 560 control subjects) explicitly reported on all critical factors in the assessment of folate. In addition, only three studies found lower plasma folate levels more frequently in patients with schizophrenia compared to controls. Further research on this topic is required to clarify the relationship between folate status and schizophrenia and should avoid the methodological pitfalls mentioned in this review. In addition, research should also focus on polymorphisms of genes related to folate metabolism.