Superoxide production from nonenzymatically glycated protein

Sakurai, Tamiko; Tsuchiya, Susumu

doi:10.1016/0014-5793(88)80066-8

Cited by 301 publications

(152 citation statements)

References 19 publications

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“…29) However, it is thought that the reduction of cytochrome c during the glycation reaction may occur by superoxide and by direct reduction from the Amadori compound. 22) Therefore superoxide anion generation during the glycation reaction has been confirmed by the SOD-dependent reduction of cytochrome c, [30][31][32][33] and the amount of superoxide formed was calculated. 22) In the present study, the incubation mixture of MG and methylglyoxal in the presence of DTPA as a chelator was found to reduce cytochrome c, and the reduction was effective in the presence of SOD.…”

Section: Discussionmentioning

confidence: 99%

Generation of Superoxide Anions during the Reaction of Guanidino Compounds with Methylglyoxal.

Nohara

Usui

Kinoshita

et al. 2002

CHEMICAL & PHARMACEUTICAL BULLETIN

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Uremic toxins are accumulated in the blood of patients with chronic renal failure (CRF), although alteration of the toxicity by the interaction of various uremic retention products has not been precisely clarified. In this study, we found that cytochrome c added to incubation mixtures containing guanidino compounds and methylglyoxal in phosphate buffer solution (pH 7.4) resulted in reduction of cytochrome c. Superoxide anions were generated from incubation mixtures of each guanidino compound with methylglyoxal, because the reduction was inhibited by the addition of superoxide dismutase. The incubation mixture containing each guanidino compound and methylglyoxal had different rates of generation of the superoxide anion from other mixtures. A relatively higher superoxide anion formation rate was observed in the incubation mixture containing Arg and methylglyoxal (7.9؎0.5 nmol · m ؊1 · min ؊1 ), or in the incubation mixture containing methylguanidine and methylglyoxal (6.3؎0.6 nmol · ml ؊1 · min ؊1). These findings suggest that interactions of various uremic retention products which accumulate in the blood of uremic patients may generate reactive oxygen species and may be involved in the oxidative stress observed in CRF patients. The addition of aminoguanidine, which is known to inhibit the formation of advanced glycation end products, to a mixture of guanidino compounds and methylglyoxal inhibited reactions between guanidino compounds and methylglyoxal.

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Section: Discussionmentioning

confidence: 99%

Generation of Superoxide Anions during the Reaction of Guanidino Compounds with Methylglyoxal.

Nohara

Usui

Kinoshita

et al. 2002

CHEMICAL & PHARMACEUTICAL BULLETIN

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“…Advanced glycation or glycosylation end products (AGEs) are the products of glycation and oxidation (glycoxidation), which are increased with age and at an accelerated rate in diabetes mellitus (9,10). In vitro studies have suggested that glycation itself may result in production of superoxide (11,12). Oxidation has been hypothesized to result in generation of superoxide, H 2 O 2 and through transition metal catalysis, hydroxyl radicals (13).…”

Section: Introductionmentioning

confidence: 99%

Protective influence of vitamin E on the antioxidant defence system in the whole blood and liver of normal and alloxan-induced diabetic rats

Olanlokun

2008

Indian J Clin Biochem

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The effect of oral administration of vitamin E for twenty-eight consecutive days on blood glucose, reduced glutathione levels, antioxidant enzymes (superoxide dismutase and catalase activities), and levels of malondialdehyde (as an index of free radical-mediated lipid peroxidation) was observed in the whole blood and liver of normal and alloxan-induced diabetic rats. It was found that oral administration of vitamin E significantly (p<0.05) lowered the blood glucose level and increased the body weight of the diabetic rats. The activities of superoxide dismutase and levels of reduced glutathione increased significantly (p<0.05) while the level of lipid peroxidation decreased.

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“…1,2) Chronic hyperglycemia induces the production of reactive oxygen species (ROS) in a great many tissues, mainly through the glycation reaction. 3,4) ROS increase in turn leads to an increase in the products of protein and DNA oxidation, as well as lipid peroxidation. 4-Hydoroxy-2-alkenals, particularly the highly cytotoxic aldehyde 4-hydroxy-2-nonenal (4-HNE), are commonly produced by the lipid peroxidation reaction and induce the production of further protein adducts as well as inducing the generation of ROS.…”

mentioning

confidence: 99%

Possible Involvement of Transient Receptor Potential Channels in Electrophile-Induced Insulin Secretion from RINm5F Cells

Numazawa

Takase

Ahiko

et al. 2012

Biological & Pharmaceutical Bulletin

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Endogenously produced reactive oxygen species reportedly stimulate insulin secretion from islet β-cells. However, the molecular machinery that governs the oxidant-induced insulin secretion has yet to be determined. The present study demonstrates, using rat islet β-cell-derived RINm5F cells, the involvement of the transient receptor potential (TRP) cation channels in the insulin secretion induced by the lipid peroxidation product 4-hydroxy-2-nonenal. Short-term (1 h) exposure of 4-hydroxy-2-nonenal induced a transient increase in intracellular Ca 2 concentration and subsequent insulin secretion in a concentration-dependent manner. The increase in intracellular Ca 2 concentration seemed to be due to an influx through the L-type voltagedependent Ca 2 channel, since it was not observed when extracellular Ca 2 was absent and was inhibited almost completely by diltiazem or nifedipine. Ruthenium red, a non-specific inhibitor of TRP channels, inhibited the Ca 2 influx and insulin secretion evoked by 4-hydroxy-2-nonenal. Among the TRP channels, TRPA1 was found to be predominantly expressed, not only in RINm5F cells, but also rat islets. TRPA1 agonists, allylisothiocyanate and 15-deoxy-Δ 12,14 -prostaglandin J 2 , significantly induced Ca 2 influx, and a specific inhibitor TRPA1, HC-030031, blocked the effects elicited by 4-hydroxy-2-nonenal. These results suggest that 4-hydroxy-2-nonenal induces Ca 2 influx via the activation of TRP channels, including TRPA1, which appears to be coupled with the L-type voltage-dependent Ca 2 channel, and ultimately insulin secretion in RINm5F cells. Key words 4-hydroxy-2-nonenal; transient receptor potential channel; islet; voltage-dependent Ca 2 channelDuring the progression of type 2 diabetes, the deterioration of insulin secretion resulting from pancreatic β-cell dysfunction leads to progressive worsening of hyperglycemia. This glucose toxicity associated with irreversible β-cell dysfunction at least in part involves the oxidative stress caused by such continuous hyperglycemia.1,2) Chronic hyperglycemia induces the production of reactive oxygen species (ROS) in a great many tissues, mainly through the glycation reaction. 3,4) ROS increase in turn leads to an increase in the products of protein and DNA oxidation, as well as lipid peroxidation. 4-Hydoroxy-2-alkenals, particularly the highly cytotoxic aldehyde 4-hydroxy-2-nonenal (4-HNE), are commonly produced by the lipid peroxidation reaction and induce the production of further protein adducts as well as inducing the generation of ROS.5) Diabetic complications have been the focus of attention with regard to ROS-mediated dysfunction, and evidence indicating pancreatic β-cells are a target of oxidative stress has been mounting. For instance, the levels of 8-hydroxy-2′-deoxyguanosine, a marker of DNA oxidation, and 4-HNEmodified proteins have been shown to be increased in the pancreatic β-cells of Goto-Kakizaki rats, 6,7) a model of nonobese Type 2 diabetes, as well as in Type 2 diabetic patients. 8)Consequently, oxidative stress origina...

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Superoxide production from nonenzymatically glycated protein

Cited by 301 publications

References 19 publications

Generation of Superoxide Anions during the Reaction of Guanidino Compounds with Methylglyoxal.

Generation of Superoxide Anions during the Reaction of Guanidino Compounds with Methylglyoxal.

Protective influence of vitamin E on the antioxidant defence system in the whole blood and liver of normal and alloxan-induced diabetic rats

Possible Involvement of Transient Receptor Potential Channels in Electrophile-Induced Insulin Secretion from RINm5F Cells

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