Obesity is associated with increased myocardial oxidative stress.
OBJECTIVE
To determine: 1) whether obesity predisposes the myocardium to oxidative stress as evidenced by higher tissue levels of myocardial lipid peroxidation, and 2) what cellular mechanisms are responsible for this predisposition.


METHODS
Comparative, descriptive study of the myocardial tissue of lean and obese Fatty Zucker animals.


METHODS
12 month old lean (-/fa; n = 6; mean body weight = 590 g) and obese (fa/fa; na = 7; mean body weight= 882 g) male Fatty Zucker rats.


METHODS
Basal lipid peroxidation (assessed using thiobarbituric reactive acid substances (TBARS) and cumene hydroperoxide equivalents), oxidative and antioxidant enzyme activities (citrate synthase (CS), superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), thiol content, heat shock protein expression (HSP72/73) and TBARS concentrations following an iron-mediated challenge in vitro.


RESULTS
Compared to lean, lipid peroxidation was greater (P < 0.05) in the left ventricle (LV) from obese rats as indicated by higher levels of lipid hydroperoxides (mean = 11.48 vs 13.7 cumene hydroperoxide equivalents (CHPE)/mg lipid) and TBARS (mean = 11.1 vs 13.9 nMol/mg lipid.). The activity of the manganese isoform of superoxide dismutase in the LV was higher (P < 0.05) in obese animals, compared to controls (mean = 135 vs 117 U/mg protein). In contrast, LV catalase and glutathione peroxidase activities did not differ (P > 0.05) between groups. Also, LV levels of HSP 72 (inducible) and 73 (constitutive) did not differ (P > 0.05)( between lean and obese animals. Following an iron-stimulated oxidative challenge in vitro, TBARS concentration was significantly greater (P < 0.05) in LV of obese rats compared to the lean (mean = 12.7 vs 16.7 nMol/mg lipid).


CONCLUSIONS
These results support the notion that obesity predisposes the myocardium to oxidative stress. However, the postulate that obesity is associated with elevated myocardial antioxidant enzyme activities and HSPs was only partially supported by these findings.
Vincent
H K
HK
Department of Exercise and Sport Sciences, Center for Exercise Science, University of Florida, Gainesville 32611, USA.
Powers
S K
SK
Stewart
D J
DJ
Shanely
R A
RA
Demirel
H
H
Naito
H
H
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight; D002352:Carrier Proteins / Q000378:metabolism; D050883:HSC70 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D011924:Rats, Zucker; D017382:Reactive Oxygen Species / Q000378:metabolism
D000975:Antioxidants; D002352:Carrier Proteins; D050883:HSC70 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C494373:Hspa8 protein, rat; D017382:Reactive Oxygen Species