Hanada K, Mitsuhashi Y, Hashimoto I
Department of Dermatology, Hirosaki University School of Medicine, Japan.
J Dermatol. 1992 Aug;19(8):456-60. doi: 10.1111/j.1346-8138.1992.tb03261.x.
In vivo experiments have shown that magnesium deficiency elicits characteristic skin lesions in the hairless rat. However, the mechanism of the involvement is not clarified. From the results of previous studies, a product derived from arachidonic acid, but not via the cyclooxygenase pathway, has been considered as an etiological cause. In this study, the inhibitory effect of newly produced leukotriene B4 (LTB4) receptor antagonist (LTBRA) against these skin manifestation was examined in hairless mutants given a hypomagnesic diet. Control animals with treatment of LTBRA developed eruptions on their bodies with increasing serum levels of LTB4, but LTBRA-treated animals did not suffer from the cutaneous disorder. Increased serum levels of LTB4 in control rats were significantly higher than those in the pre-treated condition. The diminution of skin lesions by LTBRA strongly indicated that magnesium deficiency dermatitis may involve a lipoxygenase-mediated metabolite of arachidonic acid, presumably LTB4, and that the cutaneous changes in hairless rats fed with hypomagnesic diet might provide an easily identifiable indicator of LTB4-mediated dermatitis.
体内实验表明，缺镁会在无毛大鼠身上引发特征性皮肤损伤。然而，其涉及机制尚未阐明。根据以往研究结果，一种源自花生四烯酸但并非通过环氧化酶途径产生的产物被认为是病因。在本研究中，在给予低镁饮食的无毛突变体中检测了新产生的白三烯B4（LTB4）受体拮抗剂（LTBRA）对这些皮肤表现的抑制作用。接受LTBRA治疗的对照动物随着血清LTB4水平升高身体出现皮疹，但接受LTBRA治疗的动物未患皮肤疾病。对照大鼠血清LTB4水平升高显著高于治疗前水平。LTBRA对皮肤损伤的减轻有力地表明，缺镁性皮炎可能涉及花生四烯酸的脂氧合酶介导代谢产物，推测为LTB4，并且喂食低镁饮食的无毛大鼠的皮肤变化可能为LTB4介导的皮炎提供一个易于识别的指标。
