Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles

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Abstract
Effects of a short-term vitamin E deficiency on some lipid peroxidative properties were investigated in mouse cardiac and skeletal muscles. The concentration of vitamin E decreased 35.8% in 5 wk and 61.2% in 12 wk in skeletal muscle. The corresponding decrease in cardiac muscle was 65.7% in 12 wk. Simultaneously the susceptibility of muscle homogenates to in vitro lipid peroxidation increased with 48.6% (5 wk) and 44.5% (12 wk) in skeletal muscle and with 101.8% (12 wk) in cardiac muscle. Highly significant negative correlations were observed between the concentration of vitamin E and in vitro lipid peroxidation in cardiac and skeletal muscles. Also the sensitivity to Fe2+-induced peroxidation was increased in skeletal muscle after the deficiency of 5 wk. The total contents of peroxidizable lipids (Fe2+-induction) were significantly (.apprx. 20%) decreased after 12 wk in cardiac and skeletal muscles. The concentration of lipofuscin was unaffected in both muscles of vitamin E-deficient mice. Vitamin E deficiency (5 wk) decreased the activity of Se-dependent glutathione peroxidase in skeletal muscle but did not affect the activities of catalase and .beta.-glucuronidase and the concentrations of protein, reduced glutathione and total SH groups. A short-term vitamin E deficiency affects the peroxidative properties of cardiac and skeletal muscles and may thus expose the muscles to peroxidation injuries.