Bowers R R, Lujan J, Biboso A, Kridel S, Varkey C
Department of Biology, California State University, Los Angeles 90032.
Pigment Cell Res. 1994 Dec;7(6):409-18. doi: 10.1111/j.1600-0749.1994.tb00070.x.
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.
与野生型原鸡（JF）相比，横斑洛克鸡（BPR）和白来航鸡（WL）羽毛中的黑素细胞在体内会过早死亡。由于这些突变的黑素细胞在体外能够存活，因此羽毛中的某种环境因素必定会促使它们死亡。结果表明，添加特定的抗氧化剂，如谷胱甘肽（GSH）和超氧化物歧化酶（SOD），能够在体外挽救这些处于应激条件下、会过早发生细胞死亡的突变黑素细胞。对体内GSH、过氧化氢酶和SOD水平的测量结果显示，JF、BPR和WL羽毛中的过氧化氢酶活性没有显著差异，但BPR和WL羽毛中的GSH活性均显著降低，降至JF羽毛中GSH浓度的约66%。BPR组织中的SOD活性显著降低，降至JF活性的约50%，而WL的SOD活性则显著降低，降至BPR SOD活性的约50%。谷胱甘肽过氧化物酶活性的初步测量结果表明，JF、BPR和WL羽毛中该酶的水平没有差异。基于当前结果，提出了一个关于BPR和WL羽毛黑素细胞过早细胞死亡的工作假说。BPR黑素细胞由于横斑基因（B）导致其SOD和GSH水平存在缺陷，因而具有遗传敏感性，并且由于组织液更新缓慢，氧自由基积累，在血管化不良的羽毛中，氧自由基促使其死亡。除了B基因外，WL鸡还携带显性白色基因（I）。该基因导致SOD水平进一步降低，并且与BPR鸡中已存在的细胞死亡机制相结合，使得WL羽毛黑素细胞比BPR羽毛黑素细胞更早死亡，而BPR羽毛黑素细胞又比野生型JF黑素细胞更早死亡。同样的机制假说可能是人类白癜风中黑素细胞过早死亡的原因，其中白癜风黑素细胞可能在其氧自由基保护系统中存在遗传缺陷。
