Objectives: To study the apoptosis induced by homocysteine (Hcy) and the protective effects of folic acid, VE and Se. Methods: Inverted microscopy and MTT test were used to observe the protection of these nutrients on the cytotoxic effect of Hcy. DNA agarose gel electrophoresis and flow cytometry were used to observe the inhibition of these nutrients on the apoptosis induced by Hcy. The level of MDA, the activity of SOD and GSH-Px and the generation of active oxygen in cells were also measured to investigate the mechanism of the protective effects. Results: Significant effects of folic acid, VE and Se on the protection of cell damages and the inhibition of apoptosis induced by Hcy were observed. These protective effects may be the results of decreasing MDA in cells provided by folic acid, VE and Se, increasing the activity of SOD by folic acid, increasing the activity of GSH-Px by folic acid and Se, and decreasing the generation of active oxygen by VE. Conclusions: The protective effects of folic acid, VE and Se on the damage of ECV304 cell from Hcy and the inhibitive effect on apoptosis induced by Hcy might be in different mechanisms.

A one time large dose of selenium with label was injected to Se deficient rats. Platelets, liver and PPP were assayed for GSH-Px activity and determined the uptake of Se. The results showed that platelet GSH-Px activity would also be a good index in reflecting the abrupt change of Se status. It can be changed rapidly and significantly. The results also demostrated that platelet GSH-Px trends to reflect GSH-Px in the liver which is the organ with the most labile Se pool. Platelet GSH-Px may be a suitable index of selenium status for determine the bioavilability of selenium from various food sources in short-term human studies. When different form of Se was given, GSH-Px activity in platelet, liver and PPP expressed on a protein basis was similar in the selenite and selenomethionine administered groups. However, Se uptake of platelet, liver and PPP was greater in the selenomethionine versus the selenite group, indicating that selenomethionine was being taken up nonspecifically into platelet protein other than GSH-Px. This fact was also shown by the lower platelet GSH-Px specific activity. There might be another metabolic way for Se. More work is needed to clarify metabolism of selenium in tissue.

Keshan disease was an endemic cardiomyopathy in China. The very low selenium intake of local people was considered to be an important causal factor. The main pathological characteristics of this disease was multifo-cal necrosis and fibrous replacement of myocardium that was scattered throughout the wall of all chambers.Two patterns of myocardial necrosis, myofibrillar pattern and mitochondrial pattern were distinguished in electron microscopy. The myofibrillar pattern was characterized by myofibril segmentation. It agreed well with the contraction band necrosis described in light microscopy. It was mainly seen in acute Keshan heart and might be related to circulatory disorders. Mitochondrial pattern was identical with myocytolysis of conventional pathology. It represented the typical lesion of Keshan disease.Mitochondria showed early and conspicuous changes in involved myo-cytes. Myofibrillar damage seemed to be secondary to the mitochondrial injury in the development of myocytolysis.Histochemical studies revealed that the acid phosphatase activity was obviously increased in muscle fibers surrounding the necrotic foci, and the succinic dehydrogenase activity was greatly reduced in damaged myocardio-cytes.