PREMATURE AVIAN MELANOCYTE DEATH DUE TO LOW ANTIOXIDANT LEVELS OF PROTECTION - FOWL MODEL FOR VITILIGO
PREMATURE AVIAN MELANOCYTE DEATH DUE TO LOW ANTIOXIDANT LEVELS OF PROTECTION - FOWL MODEL FOR VITILIGO
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DOI：
10.1111/j.1600-0749.1994.tb00070.x
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发表时间：
1994-12-01
期刊：
影响因子：
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通讯作者：
VARKEY, C
中科院分区：
文献类型：
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作者：
BOWERS, RR;LUJAN, J;VARKEY, C
与野生型丛林鸡（JF）相比，条纹普利茅斯岩鸡（BPR）和白来窝鸡（WL）的羽毛黑色素细胞在体内过早死亡，由于这些突变的黑色素细胞在体外存活，羽毛中的环境因素必然促成了它们的死亡。结果表明，添加抗氧化剂谷胱甘肽（GSH）和超氧化物歧化酶（SOD）可以在体外拯救这些处于应激条件下导致细胞过早死亡的突变黑色素细胞。体内GSH、过氧化氢酶和SOD水平的测量显示，JF、BPR和WL羽毛的过氧化氢酶活性没有显著差异，但BPR和WL羽毛的GSH活性显著降低，约为JF羽毛中GSH浓度的66%。BPR组织中SOD活性显著降低，约为JF活性的50%，WL SOD活性显著降低，约为BPR SOD活性的50%。谷胱甘肽过氧化物酶活性测定的初步结果表明，该酶在JF， BPR和WL羽毛中的水平没有差异。基于目前的结果，提出了BPR和WL羽毛黑素细胞过早死亡的工作假设。由于阻断基因(B)导致的SOD和GSH水平的缺陷，BPR黑素细胞在遗传上是敏感的，并且由于活性氧自由基，它们的死亡在血管化不良的羽毛中沉淀，这是由于组织液周转率低导致的氧自由基积累。白鸡除携带B基因外，还携带显性白色基因(I)。该基因指导SOD水平的进一步降低，当与BPR鸡中已经存在的细胞死亡机制结合时，导致WL羽毛黑素细胞比BPR羽毛黑素细胞早死，而BPR羽毛黑素细胞又比野生型JF黑素细胞早死。这种相同的机制假设可以应用于人类白癜风中黑色素细胞过早死亡的原因，其中白癜风黑色素细胞可能在其氧自由基保护系统中存在遗传缺陷。
Feather melanocytes in the Barred Plymouth Rock (BPR) and White Leghorn (WL) chickens die prematurely in vivo when compared to the wild type Jungle Fowl (JF) chicken, Since these mutant melanocytes live in vitro, an environmental factor in the feather must precipitate their death. Results show that the addition of selected antioxidants, glutathione (GSH) and superoxide dismutase (SOD), can rescue these mutant melanocytes in vitro that have been placed under stress conditions that cause their premature cell death. Measurements of in vivo levels of GSH, catalase, and SOD show no significant difference in catalase activity between the JF, BPR, and WL feathers but do show a significant reduction in GSH activity in both the BPR and WL feathers to approximately 66% of the GSH concentration found in JF feathers. SOD activity in the BPR tissue is reduced significantly to approximately 50% of the JF activity and the WL SOD activity is reduced significantly to approximately 50% of the BPR SOD activity. Preliminary results of measurements of glutathione peroxidase activity indicate there is no difference in the levels of this enzyme in JF, BPR and WL feathers. A working hypothesis, based on current results, is proposed for premature cell death in BPR and WL feather melanocytes. The BPR melanocytes are genetically sensitive due to a defect in their SOD and GSH levels caused by the barring gene (B) and their death, due to reactive species of oxygen radicals, is precipitated in the poorly vascularized feather by the accumulation of oxygen radicals due to the low turnover of tissue fluids. The WL chicken carries the dominant white gene (I) in addition to the B gene. This gene directs the further reduction of the level of SOD and, when combined with the cell death mechanism already present in the BPR chicken, causes the WL feather melanocytes to die much earlier than the BPR feather melanocytes which in turn die much earlier than the wild type JF melanocytes. This same mechanistic hypothesis could apply as a cause of premature melanocyte cell death in human vitiligo wherein the vitiliginous melanocytes may have a genetic defect in their oxygen radical protection system.