Toshihiko Sakanashi

Vitamin E deficiency has a pathological role in myocytolysis in cardiomyopathic Syrian hamster (BIO14.6).

This study revealed the occurrence of vitamin E deficiency in the myocardium of 60-day-old Syrian cardiomyopathic hamsters (BIO14.6), and that this deficiency might be related to the increase in lipid peroxide. Vitamin E administration for ten days effectively restored creatininekinase activity and decreased the lipid peroxide content in the myocardium, returning these to normal control levels (F1b). These results indicate that vitamin E deficiency, possibly combined with oxidative stress in the early cardiomyopathic stage plays an important role in initiating the pathogenesis of myocardial lesions.

Membrane responses of B-16 melanoma cells to single exposure to ultraviolet light

SummaryElectron spin resonance spectroscopy using the spin probe (5-, 12-and 16-deoxylstearic acid) was employed to analyze the changes in membrane fluidity in B-16 melanoma cells following UV-B exposure. The UV exposure resulted in the immediate accumulation of lipid peroxide, being accompanied by a change in membrane fluidity. The 12-DSA is the most sensitive to the changes in membrane organization caused by UV light. Na+,K+-ATPase activity was regulated by a change in membrane fluidity. Following UV exposure, the release of the prelabeled arachidonic acid from the cells was observed immediately. Ca2+-dependent calmodulin-dependent phospolipase A2-like activity was involved in the UV-stimulated arachidonic acid release from phospholipid.

Effect of UV-B irradiation on release of arachidonic acid from B-16 melanoma cells

B-16 melanoma cells in culture were prelabeled with (3H)-arachidonate, and exposed to UV radiation. Immediately after irradiation the cells released labeled materials. This UV-stimulated release was inhibited by mepacrine (20 microM) and calmodulin inhibitor W7 (0.5 microM). To determine the influence of extracellular Ca2+ on the UV-stimulated release, experiments were made with media containing various concentrations of Ca2+. The release decreased significantly at lower Ca2+ concentrations. These results suggest that Ca2+-calmodulin-dependent phospholipase A2 was involved in UV-stimulated release of radiolabeled materials, possibly arachidonic acid and its metabolites, from the cells.