title: Antioxidant changes in the hypertrophied heart due to energy metabolic disorder.
abstract: Oxidative stress has been implicated in the pathogenesis of both heart hypertrophy and heart failure. Hypertrophied heart, in response to pressure overload, is associated with an increase in antioxidant capacity and a decrease in oxidative stress. However, in the hypertrophied heart due to energy metabolic disorder, antioxidant capacity has not been investigated. Antioxidant changes in juvenile visceral steatosis (JVS) mice, a model of heart hypertrophy due to disorder of fatty-acid oxidation, were examined at 4 weeks (developing hypertrophy stage) and 8 weeks of age (established hypertrophy stage). Superoxide dismutase activity in the JVS mice was higher than that in control mice at 4 weeks of age and was not different from that in the control mice at 8 weeks of age. Glutathione peroxidase activity in the JVS mice at 8 weeks of age was lower than that in the control mice. Catalase activity showed no significant differences between the control and the JVS mice. Lipid peroxidation in the JVS mice was significantly reduced at 4 weeks of age and increased toward control levels at 8 weeks of age. The levels of vitamin E in the heart were increased in the JVS mice at 8 weeks of age. To determine whether antioxidants affect the pathogenesis of hypertrophy in this model, long-term treatments of vitamin E and 2-mercaptopropionyl glycine were performed. Vitamin E treatment partially reduced the heart hypertrophy in these mice. The present study shows that heart hypertrophy in the JVS mice is accompanied with increased antioxidant capacity as indicated in other animal models of heart hypertrophy. The precise mechanism of heart hypertrophy in JVS mice is still unknown, but oxidative stress may play a role in the pathogenesis of heart hypertrophy.
authors.affiliation: Internal Medicine II and First Department of Pathology, Nagoya University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Kamiya
authors.forename: K
authors.initials: K
authors.lastname: Okumura
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: H
authors.initials: H
authors.lastname: Matsui
authors.forename: Y
authors.initials: Y
authors.lastname: Saburi
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Hayakawa
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001794:Blood Pressure; D006332:Cardiomegaly / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D002331:Carnitine / Q000172:deficiency; D004734:Energy Metabolism / Q000502:physiology*; D005234:Fatty Liver / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006339:Heart Rate; D015227:Lipid Peroxidation / Q000502:physiology; D051379:Mice; D008809:Mice, Inbred C3H; D008817:Mice, Mutant Strains; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D009929:Organ Size; D018384:Oxidative Stress / Q000502:physiology; D013482:Superoxide Dismutase / Q000378:metabolism; D008625:Tiopronin / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology*; D024502:alpha-Tocopherol / Q000378:metabolism
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D008625:Tiopronin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D024502:alpha-Tocopherol; D002331:Carnitine