Protein and non-protein sulfhydryls and disulfides in gastric mucosa and liver after gastrotoxic chemicals and sucralfate: Possible new targets of pharmacologic agents

AIM： To investigate the role of major non-protein and protein sulfhydryls and disulfides in chemically induced gastric hemorrhagic mucosal lesions （HML） and the mechanism of gastroprotective effect of sucralfate.METHODS： Rats were given 1 mL of 75% ethanol, 25%NaCl, 0.6 mol/L HCI, 0.2 mol/L NaOH or 1% ammonia solutions intragastrically （i.g.） and sacrificed 1, 3, 6 or 12 min later. Total （reduced and oxidized） glutathione （GSH ＋ GSSG）, glutathione disulfide （GSSG）, protein free sulfhydryls （PSH）, protein-glutathione mixed disulfides （PSSG） and protein cystine disulfides （PSSP） were measured in gastric mucosa and liver.RESULTS： Reduced glutathione （GSH） was depleted in the gastric mucosa after ethanol, HCI or NaCl exposure,while oxidized glutathione （GSSG） concentrations increased, except by HCI and NaOH exposure. Decreased levels of PSH after exposure to ethanol were observed,NaCl or NaOH while the total protein disulfides were increased. Ratios of reduced to oxidized glutathione or sulfhydrils to disulfides were decreased by all chemicals.No changes in thiol homeostasis were detected in the liver after i.g. abbreviation should be spelled out the first time here administration of ethanol. Sucralfate increased the concentrations of GSH and PSH and prevented the ethanol-induced changes in gastric mucosal thiol concentrations.CONCLUSION： Our modified methods are now suitable for direct measurements of major protein and nonprotein thiols/disulfides in the gastric mucosa or liver.A common element in the pathogenesis of chemically induced HML and in the mechanism of gastroprotective drugs seems to be the decreased ratios of reduced and oxidized glutathione as well as protein sulfhydryls and disulfides.

Endogenous nitric oxide mediates alleviation of cadmium toxicity induced by calcium in rice seedlings

The effect of calcium chloride （CaCl2） on rice seedling growth under cadmium chloride （CdCl2） stress, as well as the possible role of endogenous nitric oxide （NO） in this process, was studied. The growth of rice seedlings was seriously inhibited by CdCl2, and the inhibition was significantly mitigated by CaCl2. However, hemoglobin （Hb） and 2-（4-carboxyphenyl）-4, 4,5,5-tetramethylimidazoline- l-oxyl-3-oxide （cPTIO） weakened the promotion effect of CaCl2. The results of NO fluorescence localization suggest that growth accelerated by CaCl2 might be associated with elevated NO levels. The content of Cd, protein thiols （PBT）, and nonprotein thiols （NPT） in cell walls, cell organelles, and soluble fractions, respectively, of rice seedlings decreased considerably in the presence of CaCl2, whereas the content of pectin, hemicellulose 1 （HC1）, and hemicellulose 2 （HC2） increased significantly. Elimination of endogenous NO in Cd＋Ca treatment could promote the transportation of Cd2＋ to cell organelles and soluble fractions and increase the content of NPT and PBT in leaves. In addition, transportation of Cd2＋ to cell organelles and soluble fractions was retarded in roots, the content of NPT increased, and the content of PBT decreased. With elimination of endogenous NO in Cd＋Ca treatment, the content of pectin, HC1, and HC2 decreased significantly. Thus, Ca may alleviate Cd toxicity via endogenous NO with variation in the levels of NPT, PBT, and matrix polysaccharides.