Oral zinc (Zn(2+)) is often employed for treating hair loss, even in the absence of zinc deficiency, although its mechanisms of action and efficacy are still obscure. In the current study, we explored the in vivo effects of oral zinc using the C57BL/6 mouse model for hair research. Specifically, we investigated whether continuous administration of high-dose ZnSO(4) x 7H(2)O (20 mg/ml) in drinking water affects hair follicle (HF) cycling, whether it retards or inhibits chemotherapy-induced alopecia (CIA) and whether it modulates the subsequent hair re-growth pattern. Here, we show that high doses of oral zinc significantly inhibit hair growth by retardation of anagen development. However, oral zinc also significantly retards and prolongs spontaneous, apoptosis-driven HF regression (catagen). Oral zinc can also retard, but not prevent, the onset of CIA in mice. Interestingly, Zn(2+) treatment of cyclophosphamide-damaged HFs also significantly accelerates the re-growth of normally pigmented hair shafts, which reflects a promotion of HF recovery. However, if given for a more extended time period, zinc actually retards hair re-growth. Thus, high-dose oral zinc is a powerful, yet ambivalent hair growth modulator in mice, whose ultimate effects on the HF greatly depend on the timing and duration of zinc administration. The current study also encourages one to explore whether oral zinc can mitigate chemotherapy-induced hair loss in humans and/or can stimulate hair re-growth.

High-dose oral Zn2+ is a potent downregulator of eumelanin content in murine hair shafts in vivo. The C57BL/6 mouse model offers an excellent tool for further dissecting the as yet unclear underlying molecular basis of this phenomenon, while EPR technology is well suited for the rapid, qualitative and quantitative monitoring of hair pigmentation changes.

The presence of melanin in spleens of black C57BL/6 mice has been known for long. Although its origin and biological functions are still obscure, the relation of splenic melanin to the hair follicle and skin pigmentation was suggested. Here, we demonstrated using for the first time electron paramagnetic resonance spectroscopy that black-spotted C57BL/6 spleens contain eumelanin. Its presence here is a "yes or no" phenomenon, as even in the groups which revealed the highest percentage of spots single organs completely devoid of the pigment were found. Percentage of the spotted spleens decreased, however, with the progress of telogen after spontaneously-induced hair growth. The paramagnetic properties of the spleen eumelanin differed from the hair shaft or anagen VI skin melanin. The splenic melanin revealed narrower signal, and its microwave power saturability betrayed more heterogenous population of paramagnetic centres than in the skin or hair shaft pigment. Interestingly, the pigment of dry hair shafts and of the wet tissue of depilated anagen VI skin revealed almost identical properties. The properties of splenic melanin better resembled the synthetic dopa melanin (water suspension, and to a lesser degree -- powder sample) than the skin/hair melanin. All these findings may indicate a limited degradation of splenic melanin as compared to the skin/hair pigment. The splenic eumelanin may at least in part originate from the skin melanin phagocyted in catagen by the Langerhans cells or macrophages and transported to the organ.

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Acellular (true) slime moulds (Myxomycetes) are capable of a transition to the stage of sclerotium -a dormant form of plasmodium produced under unfavourable environmental conditions. In this study, sclerotia of Fuligo septica were analyzed by means of electron paramagnetic resonance (EPR) spectroscopy. The moulds were cultivated in vitro on filter paper, fed with oat flour, and kept until the plasmodia began to produce sclerotia. The obtained sclerotia differed in colour from yellow through orange to dark-brown. The EPR spectra revealed a free radical, melanin-like signal correlated with the depth of the colour; it was strongest in the dark sclerotia. Sclerotization only took place when the plasmodia were starved and very slowly dried. Only the yellow sclerotia were able to regenerate into viable plasmodia. This suggests that myxomycete cytoplasm dehydration is an active process regulated metabolically. Plasmodial sclerotization may therefore serve as a convenient model system to study the regulation of cytoplasmatic water balance, and sclerotia as a convenient