Oxygen-derived free radicals induced cellular injury in superior mesenteric artery occlusion shock: protective effect of superoxide dismutase.
This study was designed to investigate the beneficial effect of administration of exogenous superoxide dismutase (SOD) on the inhibition of lipid peroxidation and cellular protection during superior mesenteric artery occlusion shock in rats. Wistar rats were anesthetized with sodium pentobarbital (30 mg/kg body weight), and the superior mesenteric artery occlusion shock model was induced by clamping the superior mesenteric artery for a 60-min period and then releasing the arterial clamp. The following parameters were determined: 1) average arterial blood pressure; 2) survival rate and mean survival time (MST); 3) activities of plasma lysosomal enzymes beta-glucuronidase (beta-G) and acid phosphatase (ACP); and 4) the contents of malondialdehyde (MDA) in visceral tissues. The SOD group received 15,000 U/kg body weight SOD intra-arterially 15 min before release of the clamp. The saline group received intra-arterially a corresponding volume of saline given to the SOD group. The superior mesenteric artery of rats in the control group was not clamped. In the saline group, the contents of MDA presented significant increases (P less than 0.05) in bowel and heart tissues at 1 hr after release of the clamp and showed more significant increases (P less than 0.01-0.05) in bowel, heart, liver, and lung tissues at 2 hr after release of the clamp, when compared with control values. However, the contents of MDA in bowel and heart tissues in the SOD group showed significant decreases (P less than 0.05) compared with values in the saline group and had insignificant changes (P greater than 0.05) compared with control values at 1 hr after release of the clamp. The contents of MDA in bowel, heart, and lung tissues in the SOD group were still lower than those in the saline group (P less than 0.05) at 2 hr after release of the clamp, although they were higher than those in the control group (P less than 0.05). The activities of plasma lysosomal enzymes in the SOD group were much lower than those in the saline group at 1 and 2 hr after release of the clamp. The mean survival time of shocked animals was prolonged when treated with SOD. These results suggested that administration of exogenous SOD may protect cells against lipid peroxidation injury mediated by oxygen-derived free radicals, depress the release of lysosomal enzymes, and prolong the mean survival time of shocked animals.
Research Institute of Surgery, Third Military Medical College, Chongqing, China.
J H
JH
Wang
H S
HS
Chen
T
T
Wang
Y F
YF
Diao
K L
KL
Tian
D000135:Acid Phosphatase / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D003250:Constriction; D005260:Female; D005609:Free Radicals; D005966:Glucuronidase / Q000097:blood; D015227:Lipid Peroxidation; D008247:Lysosomes / Q000201:enzymology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008638:Mesenteric Arteries; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012769:Shock / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000627:therapeutic use*
D005609:Free Radicals; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D000135:Acid Phosphatase; D005966:Glucuronidase; D010100:Oxygen