ascorbic-acid and sodium-bisulfide

Many studies have shown that hydrogen sulfide (H

Topics: Antioxidants; Ascorbic Acid; Catalase; DNA Damage; Escherichia coli; Glutathione; Hydrogen Sulfide; Oxidative Stress; Reactive Oxygen Species; Sulfides; Superoxide Dismutase

Hydrogen sulfide (H2S) has been identified as an important gaseous signal in plants. Here, we investigated the mechanism of H2S in alleviating postharvest senescence and rotting of Kyoho grape. Exogenous application of H2S released from 1.0 mM NaHS remarkably decreased the rotting and threshing rate of grape berries. H2S application also prevented the weight loss in grape clusters and inhibited the decreases in firmness, soluble solids, and titratable acidity in grape pulp during postharvest storage. The data of chlorophyll and carotenoid content suggested the role of H2S in preventing chlorophyll breakdown and carotenoid accumulation in both grape rachis and pulp. In comparison to water control, exogenous H2S application maintained significantly higher levels of ascorbic acid and flavonoid and total phenolics and reducing sugar and soluble protein in grape pulp. Meanwhile, H2S significantly reduced the accumulation of malondialdehyde (MDA), hydrogen peroxide (H2O2), and superoxide anion (O2 (∙-)) in grape pulp. Further investigations showed that H2S enhanced the activities of antioxidant enzymes ascorbate peroxidase (APX) and catalase (CAT) and decreased those of lipoxygenase (LOX) in both grape peels and pulp. In all, we provided strong evidence that H2S effectively alleviated postharvest senescence and rotting of Kyoho grape by modulating antioxidant enzymes and attenuating lipid peroxidation.

Topics: Antioxidants; Ascorbate Peroxidases; Ascorbic Acid; Carotenoids; Catalase; Cellular Senescence; Chlorophyll; Crops, Agricultural; Flavonoids; Fruit; Hydrogen Sulfide; Lipid Peroxidation; Lipoxygenase; Malondialdehyde; Oxidative Stress; Phenols; Plant Proteins; Reactive Oxygen Species; Sulfides; Time Factors; Vitis

Temperature extremes represent an important limiting factor to plant growth and productivity. The present study evaluated the effect of hydroponic pretreatment of strawberry (Fragaria x ananassa cv. 'Camarosa') roots with an H2S donor, sodium hydrosulfide (NaHS; 100 μM for 48 h), on the response of plants to acute heat shock treatment (42°C, 8 h).. Heat stress-induced phenotypic damage was ameliorated in NaHS-pretreated plants, which managed to preserve higher maximum photochemical PSII quantum yields than stressed plants. Apparent mitigating effects of H2S pretreatment were registered regarding oxidative and nitrosative secondary stress, since malondialdehyde (MDA), H2O2 and nitric oxide (NO) were quantified in lower amounts than in heat-stressed plants. In addition, NaHS pretreatment preserved ascorbate/glutathione homeostasis, as evidenced by lower ASC and GSH pool redox disturbances and enhanced transcription of ASC (GDH) and GSH biosynthetic enzymes (GS, GCS), 8 h after heat stress imposition. Furthermore, NaHS root pretreatment resulted in induction of gene expression levels of an array of protective molecules, such as enzymatic antioxidants (cAPX, CAT, MnSOD, GR), heat shock proteins (HSP70, HSP80, HSP90) and aquaporins (PIP).. Overall, we propose that H2S root pretreatment activates a coordinated network of heat shock defense-related pathways at a transcriptional level and systemically protects strawberry plants from heat shock-induced damage.

Topics: Antioxidants; Aquaporins; Ascorbic Acid; Fragaria; Gene Expression Regulation, Plant; Glutathione; Heat-Shock Proteins; Hot Temperature; Hydrogen Peroxide; Plant Proteins; Sulfides; Superoxide Dismutase

Primary cultures of rat myocardial cells were used to evaluate the cellular dynamics of calcium accumulation after exposure to isoproterenol (ISO). Non-toxic concentrations of ISO (2.4 X 10(-7) M) caused a gradual increase in myocyte calcium uptake. These effects peaked 3 min after exposure and returned to control levels within 2 min. Toxic concentrations of ISO caused a biphasic increase in calcium uptake. The initial phase peaked 1 min after exposure and returned to control levels by 3 min. A second phase was characterized by a progressive increase in calcium uptake that plateaued 10 min after exposure. Ascorbic acid (AA, 5 X 10(-3) M) and sodium bisulfite (SB, 9.6 X 10(-4) M) did not modify the calcium uptake of the initial phase, whereas propranolol (1 X 10(-6) M) and verapamil (1 X 10(-5) M) prevented the initial rise in calcium uptake. In contrast, the antioxidants prevented the the second phase of ISO-induced calcium uptake, whereas verapamil and propranolol did not. The toxic accumulation of calcium induced by ISO may be due to oxidative damage of the sarcolemma. Antioxidants may prevent the formation of oxidative metabolites from ISO and the subsequent calcium overload. Our results show that agents which modify slow calcium-channel transport do not prevent ISO-induced calcium overload in our cell culture system.

Topics: Animals; Antioxidants; Ascorbic Acid; Calcium; Cells, Cultured; Heart; Isoproterenol; Myocardium; Rats; Rats, Inbred Strains; Sulfides