Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.5 (NADH dehydrogenase)
 2,135 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Saline extracts of burn eschar (CEBE) and normal skin (CENS) caused inhibition to mitochondrial respiration and inner membrane function. Ethyl acetate extracts from CEBE (D1) and CENS (D'1) caused depression of the Respiratory Control Ratio, (RCR), an inhibition of respiration rate in state 3 and stimulation to state 4 respiration. Excellent linear correlations exist between the degree of inhibition to state 3, rate of stimulation to state 4 respiration and the logarithm of doses of D1 and D'1. The effective dose ranges (0.75-0.25 mg/ml for D1 and 4-1 mg/ml for D'1) differ by one order of magnitude. The activity of NADH dehydrogenase and succinate dehydrogenase of mitochondria after incubation with the highest toxic dose of D1 or D'1 remained normal. Dinitrophenol (DNP)-stimulated respiration was moderately inhibited by D1 and D'1. No change of oligomycin-sensitive ATPase activity was demonstrated. Exogenous malondialdehyde (MDA) did not show any inhibitory effect. Preliminary studies show that D1 contains a family of free fatty acids (FFA). Incubation of normal mitochondria with D1 increased the content of saturated FFA and a decrease of unsaturated FFA. The role of other peroxidative products is under investigation.
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PMID:Inhibition of mitochondrial respiratory function by an organic solvent extractable component from an extract of burn eschar. 183 77

Salt stress threatens the achievement of sustainable global food security goals by inducing secondary stresses, such as osmotic, ionic, and oxidative stress, that are detrimental to plant growth and productivity. Various studies have reported the beneficial roles of microbes in ameliorating salt stress in plants. This review emphasizes salt tolerance and endurance mechanisms (STEM) in microbially inoculated (MI) plants that ensure plant growth and survival. Well-established STEM have been documented in MI plants and include conglomeration of osmolytes, antioxidant barricading, recuperating nutritional status, and ionic homeostasis. This is achieved via involvement of P solubilization, siderophore production, nitrogen fixation, selective ion absorption, volatile organic compound production, exopolysaccharide production, modifications to plant physiological processes (photosynthesis, transpiration, and stomatal conductance), and molecular alterations to alter various biochemical and physiological processes. Salt tolerance and endurance mechanism in MI plants ensures plant growth by improving nutrient uptake and maintaining ionic homeostasis, promoting superior water use efficiency and osmoprotection, enhancing photosynthetic efficiency, preserving cell ultrastructure, and reinforcing antioxidant metabolism. Molecular research in MI plants under salt stress conditions has found variations in the expression profiles of genes such as HKT1, NHX, and SOS1 (ion transporters), PIPs and TIPs (aquaporins), RBCS, RBCL (RuBisCo subunits), Lipoxygenase2 [jasmonic acid (JA) signaling], ABA (abscisic acid)-responsive gene, and APX, CAT, and POD (involved in antioxidant defense). Proteomic analysis in arbuscular mycorrhizal fungi-inoculated plants revealed upregulated expression of signal transduction proteins, including Ca2+ transporter ATPase, calcium-dependent protein kinase, calmodulin, and energy-related proteins (NADH dehydrogenase, iron-sulfur protein NADH dehydrogenase, cytochrome C oxidase, and ATP synthase). Future research should focus on the role of stress hormones, such as JA, salicylic acid, and brassinosteroids, in salt-stressed MI plants and how MI affects the cell wall, secondary metabolism, and signal transduction in host plants.
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PMID:Insights Into Microbially Induced Salt Tolerance and Endurance Mechanisms (STEM) in Plants. 3298 94