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Cardiac‐specific overexpression of catalase prolongs survival and attenuates paraquat‐induced myocardial contractile dysfunction
Author(s) -
GE WEI,
MA HENG,
ZHANG YINGMEI,
HAN XUEFENG,
REN JUN
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.575.3
Subject(s) - paraquat , catalase , cardiac function curve , reactive oxygen species , antioxidant , transgene , medicine , chemistry , oxidative stress , endocrinology , andrology , biochemistry , heart failure , gene
Paraquat, a quarternary nitrogen herbicide, is highly toxic for humans and animals via generation of reactive oxygen species. This study was designed to examine the influence of cardiac‐specific overexpression of catalase (CAT), an antioxidant enzyme responsible for detoxification of H2O2 on murine myocardial contractile function following the challenge of the pro‐oxidant paraquat. FVB and CAT mice were administrated paraquat (75 mg/kg) and myocardial function was monitored with echocardiography and edge‐detection. Cardiomyocyte mechanical indices analyzed included peak shortening (PS), time‐to‐PS (TPS), time‐to‐90% relengthening (TR90), and maximal velocity of shortening/relengthening (+/‐dL/dt). Our results revealed that CAT mice displayed a significantly improved survival against paraquat‐induced death than FVB mice as evaluated by the Kaplan‐Meier curve. The CAT transgene itself did not alter cardiac function. Paraquat treatment for 48 hours enlarged end‐systolic diameter, reduced fractional shortening, PS and +/− dL/dt in FVB group. Interestingly, all these defects were nullified or significantly attenuated by CAT. Taken together, our data revealed that CAT overexpression may rescue paraquat‐induced decrease in survival, myocardial contractile dysfunction.