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Lactoylglutathione lyase

About: Lactoylglutathione lyase is a research topic. Over the lifetime, 771 publications have been published within this topic receiving 35158 citations. The topic is also known as: GLOD1 & GLYI.


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Journal ArticleDOI
TL;DR: Results suggest that both ascorbate and glutathione homeostasis can be considered as biomarkers for salt tolerance in Pokkali rice and status of reactive oxygen species and oxidative DNA damage can serve as a quick and sensitive biomarker for screening against salt and other abiotic stresses in crop plants.
Abstract: To identify biochemical markers for salt tolerance, two contrasting cultivars of rice (Oryza sativa L.) differing in salt tolerance were analyzed for various parameters. Pokkali, a salt-tolerant cultivar, showed considerably lower level of H(2)O(2) as compared to IR64, a sensitive cultivar, and such a physiology may be ascribed to the higher activity of enzymes in Pokkali, which either directly or indirectly are involved in the detoxification of H(2)O(2). Enzyme activities and the isoenzyme pattern of antioxidant enzymes also showed higher activity of different types and forms in Pokkali as compared to IR64, suggesting that Pokkali possesses a more efficient antioxidant defense system to cope up with salt-induced oxidative stress. Further, Pokkali exhibited a higher GSH/GSSG ratio along with a higher ratio of reduced ascorbate/oxidized ascorbate as compared to IR64 under NaCl stress. In addition, the activity of methylglyoxal detoxification system (glyoxalase I and II) was significantly higher in Pokkali as compared to IR64. As reduced glutathione is involved in the ascorbate-glutathione pathway as well as in the methylglyoxal detoxification pathway, it may be a point of interaction between these two. Our results suggest that both ascorbate and glutathione homeostasis, modulated also via glyoxalase enzymes, can be considered as biomarkers for salt tolerance in Pokkali rice. In addition, status of reactive oxygen species and oxidative DNA damage can serve as a quick and sensitive biomarker for screening against salt and other abiotic stresses in crop plants.

257 citations

Journal ArticleDOI
01 Jul 2006-Diabetes
TL;DR: It is shown that increased modification of vascular basement membrane type IV collagen by methylglyoxal, a dicarbonyl glycating agent with increased formation in hyperglycemia, caused endothelial cell detachment, anoikis, and inhibition of angiogenesis, and likely contributes to similar vascular dysfunction in diabetes.
Abstract: Chronic vascular disease in diabetes is associated with disruption of extracellular matrix (ECM) interactions with adherent endothelial cells, compromising cell survival and impairing vasculature structure. Loss of functional contact with integrins activates anoikis and impairs angiogenesis. The metabolic dysfunction underlying this vascular damage and disruption is unclear. Here, we show that increased modification of vascular basement membrane type IV collagen by methylglyoxal, a dicarbonyl glycating agent with increased formation in hyperglycemia, formed arginine-derived hydroimidazolone residues at hotspot modification sites in RGD and GFOGER integrin-binding sites of collagen, causing endothelial cell detachment, anoikis, and inhibition of angiogenesis. Endothelial cells incubated in model hyperglycemia in vitro and experimental diabetes in vivo produced the same modifications of vascular collagen, inducing similar responses. Pharmacological scavenging of methylglyoxal prevented anoikis and maintained angiogenesis, and inhibition of methylglyoxal metabolism with a cell permeable glyoxalase I inhibitor provoked these responses in normoglycemia. Thus, increased formation of methylglyoxal and ECM glycation in hyperglycemia impairs endothelial cell survival and angiogenesis and likely contributes to similar vascular dysfunction in diabetes.

254 citations

Journal ArticleDOI
TL;DR: Analysis of a methylglyoxal synthase-deficient mutant provides evidence that methylgly oxal production is required to allow growth under certain environmental conditions, and may represent a high-risk strategy that facilitates adaptation, but which on failure leads to cell death.
Abstract: Methylglyoxal is a toxic electrophile. In Escherichia coli cells, the principal route of methylglyoxal production is from dihydroxyacetone phosphate by the action of methylglyoxal synthase. The toxicity of methylglyoxal is believed to be due to its ability to interact with the nucleophilic centres of macromolecules such as DNA. Bacteria possess an array of detoxification pathways for methylglyoxal. In E. coli, glutathione-based detoxification is central to survival of exposure to methylglyoxal. The glutathione-dependent glyoxalase I-II pathway is the primary route of methylglyoxal detoxification, and the glutathione conjugates formed can activate the KefB and KefC potassium channels. The activation of these channels leads to a lowering of the intracellular pH of the bacterial cell, which protects against the toxic effects of electrophiles. In addition to the KefB and KefC systems, E. coli cells are equipped with a number of independent protective mechanisms whose purpose appears to be directed at ensuring the integrity of the DNA. A model of how these protective mechanisms function will be presented. The production of methylglyoxal by cells is a paradox that can be resolved by assigning an important role in adaptation to conditions of nutrient imbalance. Analysis of a methylglyoxal synthase-deficient mutant provides evidence that methylglyoxal production is required to allow growth under certain environmental conditions. The production of methylglyoxal may represent a high-risk strategy that facilitates adaptation, but which on failure leads to cell death. New strategies for antibacterial therapy may be based on undermining the detoxification and defence mechanisms coupled with deregulation of methylglyoxal synthesis.

249 citations

Journal ArticleDOI
TL;DR: Investigation of the regulatory role of exogenous selenium in the antioxidant defense and methylglyoxal (MG) detoxification systems in rapeseed seedlings exposed to salt stress suggests that the exogenous application of Se rendered the plants more tolerant to salt Stress-induced oxidative damage by enhancing their antioxidants defense and MG detoxification system.
Abstract: The present study investigates the regulatory role of exogenous selenium (Se) in the antioxidant defense and methylglyoxal (MG) detoxification systems in rapeseed seedlings exposed to salt stress. Twelve-day-old seedlings, grown in Petri dishes, were supplemented with selenium (25 μM Na2SeO4) and salt (100 and 200 mM NaCl) separately and in combination, and further grown for 48 h. The ascorbate (AsA) content of the seedlings decreased significantly with increased salt stress. The amount of reduced glutathione (GSH) and glutathione disulfide (GSSG) increased with an increase in the level of salt stress, while the GSH/GSSG ratio decreased. In addition, the ascorbate peroxidase (APX) and glutathione S-transferase (GST) activity increased significantly with increased salt concentration (both at 100 and 200 mM NaCl), while glutathione peroxidase (GPX) activity increased only at moderate salt stress (100 mM NaCl). Glutathione reductase (GR) activity remained unchanged at 100 mM NaCl, while it was decreased under severe (200 mM NaCl) salt stress. Monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), catalase (CAT), glyoxalase I (Gly I), and glyoxalase II (Gly II) activities decreased upon the imposition of salt stress, whereas a sharp decrease of these activities was observed under severe salt stress (200 mM NaCl). Concomitant increases in the levels of H2O2 and lipid peroxidation (MDA) were also measured. Exogenous Se treatment alone had little effect on the non-enzymatic and enzymatic components. However, further investigation revealed that Se treatment had a synergistic effect: in salt-stressed seedlings, it increased the AsA and GSH contents; GSH/GSSG ratio; and the activities of APX, MDHAR, DHAR, GR, GST, GPX, CAT, Gly I, and Gly II. As a result, addition of Se in salt-stressed seedlings led to a reduction in the levels of H2O2 and MDA as compared to salt stress alone. These results suggest that the exogenous application of Se rendered the plants more tolerant to salt stress-induced oxidative damage by enhancing their antioxidant defense and MG detoxification systems.

248 citations

Journal ArticleDOI
TL;DR: The 2-oxoaldehyde methylglyoxal (MeG) is the precursor to a number of the known advanced glycation endproducts (AGE) implicated in the development of diabetic complications, and rates of production of MeG depend upon physiological conditions such as hyperglycemia and ketoacidosis.

242 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202310
202242
202119
202028
201919
201823