Premature Avian Melanocyte Death Due to Low Antioxidant Levels of Protection: Fowl Model for Vitiligo

Abstract

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 (1) 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.

Dietary flavonoids enhance conspicuousness of a melanin‐based trait in male blackcaps but not of the female homologous trait or of sexually monochromatic traits

“…Flavonoids may enhance melanin deposition in feathers by two different mechanisms: first, flavonoids are strong antioxidants in vitro that may enhance consumer body condition and melanocyte development by reducing oxidative stress (Bowers et al. , 1994, 1999; Arck et al.…”

“…, 2008a). Flavonoids may also increase calcium availability and reduce oxidative stress, both important factors that may enhance melanin synthesis (Bowers et al. , 1994, 1999; Arck et al.…”

Hyperpigmentation in the Silkie fowl correlates with abnormal migration of fate-restricted melanoblasts and loss of environmental barrier molecules

“…We used LBL birds for this aspect of the study, because WLH melanoblasts die before they become fully differentiated (Jimbow et al, 1974;Bowers et al, 1994).…”

Sex‐linked barring in chickens is controlled by the CDKN2A /B tumour suppressor locus

“…During the formation of the white bands of a BPR feather, few, if any, melanocytes were observed, and cell culture experiments showed that BPR feather melanocytes died approximately five times earlier than wild‐type feather melanocytes. More recently, the same group reported that melanocytes from sex‐linked barred feathers were more sensitive to oxidative stress than those of wild‐type chickens (Bowers et al., 1994). They proposed that in Sex‐linked barring individuals, melanocytes die due the high levels of reactive oxygen species (ROS) present during pigment production, and when ROS levels decrease, pigmentation progresses normally until there is again an increase in ROS levels.…”