Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles.
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 weeks and 61.2% in 12 weeks in skeletal muscle. The corresponding decrease in cardiac muscle was 65.7% in 12 weeks. Simultaneously the susceptibility of muscle homogenates to in vitro lipid peroxidation increased with 48.6% (5 weeks) and 44.5% (12 weeks) in skeletal muscle and with 101.8% (12 weeks) 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 weeks. The total contents of peroxidizable lipids (Fe2+-induction) were significantly (approx. 20%) decreased after 12 weeks in cardiac and skeletal muscles. The concentration of lipofuscin was unaffected in both muscles of vitamin E-deficient mice. Vitamin E deficiency (5 weeks) decreased the activity of selenium-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 sulfhydryl groups. These results show that a short-term vitamin E deficiency affects the peroxidative properties of cardiac and skeletal muscles and may thus expose the muscles to peroxidation injuries.
D000818:Animals; D050356:Lipid Metabolism; D008062:Lipofuscin / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009132:Muscles / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D013997:Time Factors; D014810:Vitamin E / Q000378:metabolism; D014811:Vitamin E Deficiency / Q000378:metabolism*
D008062:Lipofuscin; D014810:Vitamin E