Effect of streptozotocin on erythrocyte and retinal superoxide dismutase

Crouch, Rosalie K.; Kimsey, Gary; Priest, David G.; Sarda, Alain; Buse, Maria G.

doi:10.1007/bf01219329

Cited by 60 publications

(32 citation statements)

References 20 publications

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“…From these results, it is most likely that the activity of SOD in the aorta is decreased in the diabetic state. Indeed, it has been found that the activity of SOD in various tissues is decreased in the diabetic state (Crouch et al, 1978;Loven et al, 1982; Matkovics et al, 1982;Cohen, 1995). On the other hand, it has been shown that hydrogen peroxide accelerates NO release (Rubanyi & Vanhoutte, 1986b), activates soluble guanylate cyclase activity, and causes smooth muscle relaxation (Zembowicz et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Changes in superoxide dismutase mRNA expression by streptozotocin‐induced diabetes

Kamata

Kobayashi

1996

British J Pharmacology

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Experiments were designed to investigate the involvement of superoxide anions in the attenuated endothelium‐dependent relaxation of the rat aorta from streptozotocin (STZ)‐induced diabetic rats. The endothelium‐dependent relaxation responses to acetylcholine (ACh, 10−7 m) in helical strips of the aorta precontracted with noradrenaline (NA, 5 × 10−8∼3 × 10−7 m) were significantly decreased in STZ‐induced diabetic rats. The recovery phase of the relaxation after single administration of ACh in the STZ‐induced diabetic rats was more rapid than those in control vessels. Preincubation of aortic strips with superoxide dismutase (SOD, 60 u ml−1) normalized the recovery phase of the relaxation of diabetic aorta after single administration of ACh, whereas catalase (150 u ml−1) or indomethacin (10−5 m) had no effects on the relaxation. SOD (180 u ml−1) caused relaxation in NA precontracted aortic strips and the degree of the SOD‐induced relaxation was significantly greater in diabetic aorta as compared with age‐matched control vessels. When the changes in mRNA expressions of Mn‐SOD or Cu‐Zn‐SOD were observed, Mn‐SOD mRNA expression was markedly decreased, and Cu‐Zn‐SOD was slightly decreased in diabetic aorta. These results suggest that the rapid destruction of NO by superoxide anions may occur in the STZ‐induced diabetic rats, and this may be due to a decrease in mRNA expression of Mn‐SOD or Cu‐Zn‐SOD.

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Section: Discussionmentioning

confidence: 99%

Changes in superoxide dismutase mRNA expression by streptozotocin‐induced diabetes

Kamata

Kobayashi

1996

British J Pharmacology

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“…The in vitro inhibition was shown with the purified erythrocyte enzyme as well as with intact erythrocytes or the enzyme extracted from islets. The in vivo inhibition was relatively tissue specific and was observed in erythrocytes and retinae of the rat after injection of streptozotocin or alloxan but not in a number of other tissues studied (5). No information is available concerning the in vivo effects of diabetogenic agents…”

Section: Introductionmentioning

confidence: 99%

Protective Role of Superoxide Dismutase against Diabetogenic Drugs

Gandy¹,

Buse²,

Crouch³

1982

J. Clin. Invest.

125

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A B S T R A C T Copper-zinc superoxide dismutase (SOD) is present in relatively high concentrations in the ,-cells of human islets. The activity of the extracted enzyme is partially inhibited upon incubation with the diabetogenic drugs alloxan, streptozotocin, or Vacor. The role of this enzyme in protecting a-cells against chemically induced diabetes was further investigated.Incubation of intact canine islets with alloxan (0.2 mg/ml) and 4 mM glucose decreased the insulin secretory response by 87% during subsequent exposure to 28 mM glucose. Concomitantly the SOD-specific activity (units of enzyme activity per milligram immunoreactive SOD) decreased 50% in alloxan-exposed islets. When islets were protected from alloxan toxicity by including 28 mM glucose with alloxan, the insulin secretory response and SOD specific activity remained identical to controls. Thus, SOD specific activity correlates with maintenance of ,B-cell function.To test the effectiveness of SOD against streptozotocin in vitro, canine islets were incubated 10 min with or without streptozotocin (0.1 mg/ml) with 4 mM glucose; their functional integrity was tested subsequently as the insulin secretory response to 28 mM glucose. Exposure to streptozotocin alone decreased the response by 70%; inclusion of SOD (1.5 mg/ml) before and during exposure to streptozotocin completely prevented this effect. Cyanide-inactivated SOD was not effective.The potential of SOD to prevent streptozotocin-induced diabetes was tested in rats in vivo. SOD injected 10 s or 50 min before streptozotocin prevented or significantly attenuated diabetes. Injection of SOD and streptozotocin simultaneously was much less effective, and cyanide-inactivated SOP was ineffective. No protection was afforded by injection of SOD 12 or 24 h before streptozotocin.

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“…For example, endogenous antioxidant and scavenging protectors such as vitamin E and glutathione are depleted in diabetes and antioxidant enzymes such as superoxide dismutase and catalase are less active [15][16][17][18].…”

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confidence: 99%