Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.3 (complex I)
 8,901 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of complex I has been considered to be an important contributor to mitochondrial dysfunction in tissues subjected to ischemia-reperfusion. We have investigated the role of complex I in a severe energetic deficit that develops in kidney proximal tubules subjected to hypoxia-reoxygenation and is strongly ameliorated by supplementation with specific citric acid cycle metabolites, including succinate and the combination of -ketoglutarate plus malate. NADH: ubiquinone reductase activity in the tubules was decreased by only 26% during 60-min hypoxia and did not change further during 60-min reoxygenation. During titration of complex I activity with rotenone, progressive reduction of NAD+ to NADH was detected at >20% complex I inhibition, but substantial decreases in ATP levels and mitochondrial membrane potential did not occur until >70% inhibition. NAD+ was reduced to NADH during hypoxia, but the NADH formed was fully reoxidized during reoxygenation, consistent with the conclusion that complex I function was not limiting for recovery. Extensive degradation of cytosolic and mitochondrial NAD(H) pools occurred during either hypoxia or severe electron transport inhibition by rotenone, with patterns of metabolite accumulation consistent with catabolism by both NAD+ glycohydrolase and pyrophosphatase. This degradation was strongly blocked by alpha-ketoglutarate plus malate. The data demonstrate surprisingly little sensitivity of these cells to inhibition of complex I and high levels of resistance to development of complex I dysfunction during hypoxia-reoxygenation and indicate that events upstream of complex I are important for the energetic deficit. The work provides new insight into fundamental aspects of mitochondrial pathophysiology in proximal tubules during acute renal failure.
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PMID:Preservation of complex I function during hypoxia-reoxygenation-induced mitochondrial injury in proximal tubules. 1466 31

Drought stress negatively influences the growth and physiology of perennial grasses. The objective of this study was to identify associations of candidate genes with drought tolerance traits in 96 zoysiagrass (Zoysia Willd.) accessions. Germplasm varied largely in leaf wilting, canopy and air temperature difference (CAD), leaf water content (LWC), chlorophyll fluorescence (Fv/Fm), leaf dry weight (LDW), stolon dry weight (SDW), rhizome dry weight (RZW), and root dry weight (RDW) under drought stress across the two experiments in 2014 and 2015 in a greenhouse. The population exhibited three subgroups based on molecular marker analysis and had minimum relative kinship. Associations between single nucleotide polymorphisms (SNPs) in BADH encoding betaine aldehyde dehydrogenase, DREB1 encoding DREB-like protein 1, Ndhf encoding NADH dehydrogenase subunit F, CAT encoding catalase, and VP1 encoding H+-pyrophosphatase were analyzed with trait under drought stress (D) and relative values compared to the control (R). Twenty-seven mark and trait associations were detected in year 2014, 2015, and a two-year combination across four genes, including 13 associations in 7 SNP loci in BADH, 9 associations in 5 SNP loci in DREB1, 3 associations in one SNP locus in Ndhf, and 2 associations in one SNP locus in CAT. Of them, one SNP in BADH was associated with D-RDW or D-SDW, three SNPs in DREB1 were associated with D-RZW, D-RDW, R-LWC, and D-CAD, and one SNP in CAT was associated with D-SDW. Nucleotide changes in these SNP loci caused non-synonymous amino acid substitutions. The results indicated that allelic diversity in genes involved in antioxidant metabolism, osmotic homeostasis, and dehydration responsive transcription factor could contribute to growth and physiological variations in zoysiagrass under drought stress.
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PMID:Association of candidate genes with drought tolerance traits in zoysiagrass germplasm. 3102 77