Inhibition of the glycolytic pathway by methylglyoxal in human platelets

Leoncini, Giuliana; Maresca, M; Buzzi, E

doi:10.1002/cbf.290070111

Cited by 53 publications

(22 citation statements)

References 12 publications

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“…Methylglyoxal has been shown to decrease the level of protein thiol ( Baskaran & Balasubramanian 1990) and reduced glutathione GSH ( Kalapos et al . 1991 ;Leoncini et al . 1989 ).…”

Section: Discussionmentioning

confidence: 99%

Glyoxalase I fromBrassica juncea: molecular cloning, regulation and its over‐expression confer tolerance in transgenic tobacco under stress

1999

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SummaryDespite its ubiquitous presence, the role of glyoxalase I has not been well investigated in plants. In order to find out its physiological functions, we have cloned and characterized a cDNA from Brassica juncea encoding glyoxalase I (Gly I) and made transgenic tobacco plants harbouring Gly I in both sense and antisense orientation. The transgenic nature of the plants was confirmed by Southern blotting, and the estimated number of genes inserted ranged from one to six. The transcript and protein levels of glyoxalase I were also monitored in transgenic plants. The expression of glyoxalase I in B. juncea was upregulated in response to salt, water and heavy metal stresses. In response to a high concentration of salt, the transcript level averaged threefold higher in 72 h, and an increase in the protein was also seen by immunoblotting. The transgenic plants over-expressing glyoxalase I showed significant tolerance to methylglyoxal and high salt, as tested in detached leaf disc senescence assay. A comparison of plants expressing high and low levels of glyoxalase I showed that the tolerance to different salt concentrations was correlated with the degree of glyoxalase I expression. Our results suggest an important role of glyoxalase I in conferring tolerance to plants under stress conditions.

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“…Methylglyoxal has been shown to decrease the level of protein thiol ( Baskaran & Balasubramanian 1990) and reduced glutathione GSH ( Kalapos et al . 1991 ;Leoncini et al . 1989 ).…”

Section: Discussionmentioning

confidence: 99%

Glyoxalase I fromBrassica juncea: molecular cloning, regulation and its over‐expression confer tolerance in transgenic tobacco under stress

1999

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“…GAPDH, a key glycolytic enzyme, is sensitive to inhibition by agents of oxidative stress such as superoxide radicals and H 2 O 2 (64). Of all the glycolytic enzymes, only GAPDH has been shown to be inhibited by H 2 O 2 in cardiac muscle (65).…”

Section: Role Of Methylglyoxal In Hypertensionmentioning

confidence: 99%

Role of methylglyoxal in essential hypertension

Vasdev

Stuckless²

2010

Int J Angiol

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Altered glucose metabolism due to insulin resistance is a common feature of essential hypertension in humans and in animal models. Elevated endogenous aldehydes in genetic (spontaneously hypertensive rats) and acquired (fructose-induced hypertensive rats) models of essential hypertension may be due to increased production of the reactive aldehyde methylglyoxal, resulting from altered glucose metabolism. Excess methylglyoxal binds sulfhydryl groups of membrane proteins, altering calcium channels and increasing cytosolic free Ca(2+) and blood pressure. It has been demonstrated that methylglyoxal, when given in drinking water to Wistar-Kyoto rats, leads to an increase in kidney aldehyde conjugates, cytosolic free Ca(2+) concentration, decreased serum nitric oxide, renal vascular hyperplasia and hypertension. N-acetylcysteine (NAC) in the diet of these animals prevented hypertension and associated biochemical and morphological changes. NAC normalizes blood pressure by directly binding to excess methylglyoxal, thus normalizing Ca(2+) channels, cytosolic Ca(2+) and nitric oxide. NAC also leads to increased levels of tissue glutathione, a storage form of cysteine. Glutathione acts as a cofactor in the enzymatic catabolism of methylglyoxal. Cysteine and other antioxidants, such as vitamins B(6), C and E, and lipoic acid, prevented hypertension and associated biochemical and morphological changes in both genetic and acquired rat models of hypertension. The antihypertensive effect of dietary antioxidants may be due to an increase in tissue cysteine and glutathione, which improves glucose metabolism and decreases tissue methylglyoxal. A diet rich in these antioxidants may be effective in preventing and controlling hypertension in humans.

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“…Methylglyoxal reacts with arginine and arginyl residues in proteins (Takahashi, 1977a,b;Cheung & Fonda, 1979). Methylglyoxal (> 10 mM) inhibits glycolytic enzymes (Leonici et al, 1989) and inhibits microtubule assembly (Miglietta & Gabriel, 1986). Since estimates of the physiological concentration of methylglyoxal are in the range 0.1-2 ,UM (Ohmori et al, 1987b;Thornalley et al, 1988), these effects on protein function are expected to be of little physiological significance.…”

Section: Reaction Of Methylglyoxal With Biological Moleculesmentioning

confidence: 99%