A common feature of Parkinson’s disease (PD) and melanoma is their starting points being based on cells capable of converting tyrosine into melanin. Melanocytes produce two types of melanin: eumelanin and pheomelanin. These dyes are designed to protect epidermal cells from the harmful effects of UV radiation. Neurones of the substantia nigra, which degenerate during PD, produce neuromelanin, the physiological role of which is not fully explained. This article discusses the potential role of melanins in the pathogenesis of both diseases. Melanins, due to their ability to accumulate toxic substances, may become their sources over time. The use of glutathione for the synthesis of pheomelanins and neuromelanins may reduce the antioxidant capacity of cells, leading to an excessive synthesis of free radicals. This study also tested the hypothesis that certain drugs used in the treatment of PD (L-DOPA, MAO-B and COMT inhibitors, and amantadine), aimed at increasing dopamine concentration, could potentially contribute to the development of melanoma. The role and properties of melanins should continue to be researched. Whether excessive melanin synthesis or its accumulation in the extracellular space may be factors initiating the development of diseases remains an open question.
帕金森病(PD)与黑色素瘤的共同特征在于其发病基础均源于能够将酪氨酸转化为黑色素的细胞。黑色素细胞可产生两种类型的黑色素:真黑素与褐黑素。这些色素旨在保护表皮细胞免受紫外线辐射的有害影响。在帕金森病中发生退行性变的黑质神经元会产生神经黑色素,其生理作用尚未得到完全阐明。本文探讨了黑色素在这两种疾病发病机制中的潜在作用。由于黑色素具有蓄积毒性物质的能力,随时间推移可能成为毒性物质的来源。谷胱甘肽参与褐黑素和神经黑色素的合成过程,可能降低细胞的抗氧化能力,导致自由基的过度生成。本研究还验证了以下假设:某些用于治疗帕金森病的药物(左旋多巴、单胺氧化酶B抑制剂、儿茶酚-O-甲基转移酶抑制剂及金刚烷胺)旨在提高多巴胺浓度,但可能潜在地促进黑色素瘤的发展。黑色素的作用与特性仍需持续深入研究。黑色素的过度合成或其细胞外间隙的蓄积是否可能成为疾病发生的启动因素,目前仍是一个有待解答的问题。
Melanin—The Éminence Grise of Melanoma and Parkinson’s Disease Development