Abstract
Vitamin B12 deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B12 deficiency, however the cellular and molecular mechanisms underlying these effects remain unknown. The aim of this study was to examine the effect of vitamin B12 deficiency on melanocytes homeostasis. Hypocobalaminemia in vitro model was developed by treating epidermal melanocytes with synthesized vitamin B12 antagonist—hydroxycobalamin(c-lactam). The cells were examined using immunoenzymatic, spectrophotometric, and fluorimetric assays as well as image cytometry. Significant melanogenesis stimulation—the increase of relative melanin content and tyrosinase activity up to 131% and 135%, respectively—has been indicated. Cobalamin-deficient cells displayed the elevation (by 120%) in reactive oxygen species level. Moreover, the redox status imbalance was stated. The study provided a scientific evidence for melanocytes homeostasis disturbance under hypocobalaminemia, thus indicating a significant element of the hyperpigmentation mechanism due to vitamin B12 deficiency. Furthermore, the implication between pigmentary and hematological and/or neuropsychiatric symptoms in cobalamin-deficient patients may be an important issue.
Highlights
Vitamin B12 deficiency is an important health issue, among the elderly
Vitamin B12 deficiency causes significant changes in cellular metabolism leading to various clinical symptoms [1,11]
Our results showed that long-term incubation of human melanocytes with (OH)Cbl(c-lactam) in concentration of 10 μg/mL only slightly affected the cell viability (Figure 2a)
Summary
Vitamin B12 (cobalamin) deficiency is an important health issue, among the elderly. The main causes of hypocobalaminemia are insufficient dietary intake (e.g., in vegans and vegetarians) and malabsorption of the vitamin [1]. Vitamin B12 plays a key role in cellular metabolism. It is a cofactor of two enzymes: Methionine synthase, which catalyzes a methylation of homocysteine to methionine with simultaneous reconstitution of tetrahydrofolate and methylmalonyl-CoA mutase, which catalyzes the conversion of methylmalonyl-CoA to succinyl-CoA. Cobalamin deficiency results in the inhibition of purine synthesis and in the accumulation of methylmalonic acid and homocysteine (Hcy) [1]. Hcy has been previously demonstrated to act as a prooxidant in various types of cells [3,4]
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