Elevated plasma homocysteine is a risk factor for atherosclerotic disease. In the present study, we have examined whether the oxidative stress due to a low level of vitamin B₆ accelerates the development of homocysteine-induced atherosclerosis in rats. First, the effect of homocysteine thiolactone intake (50mg/kgperd) on vascular integrity, lipid peroxide concentration, endothelial NO synthase (eNOS) expression and biochemical profiles was examined at day 1, day 21 and day 42 (five rats per group). The histochemical staining ofthe rat aorta showed no change at day 1 and day 21, but the subendothelial space was observed to be enlarged in rat aorta at day 42 with exposure to homocysteine thiolactone. Expression of eNOS was observed in rat aorta at day 42, but not at day 1 and day 21. Serum lipid peroxide concentration and biochemical profiles including glucose cholesterol and triacylglycerol showed no change at any day. Second, the effect of homocysteine thiolactone intake in the presence and absence of vitamin B₆ on vascular integrity was examined at day 1 and day 14 (five rats per group). Aortic lesions were observed in vitamin B₆-deficient rat aorta at day 14 but not in vitamin B₆-supplemented rats. The expression of eNOS was also observedin vitamin B₆-deficient rat aorta at day 14. Serum lipid concentrations of the vitamin B₆-deficient group significantly increased compared with concentrations of the vitamin B₆-supplemented group, though serum concentration of homocysteine did not change between both groups. These results suggest that the oxidative stress caused by a low level of vitamin B₆ accelerates the development of homocysteine-induced atherosclerosis in rats.

A keratinolytic alkaline proteae (NAPase) from Nocardiopsis sp. TOA-1 degraded a scrapie prion without any chemical or physical treatment. Optimal temperature and pH were 60 degrees C and above pH 10.0. The scrapie prion was completely degraded within 3 min under optimal conditions.