Modulation of nickel toxicity by glycinebetaine and aspirin in Pennisetum typhoideum

Germinated Pennisetum typhoideum seeds were grown under phytotoxic amount of nickel (Ni) and its combinations with aspirin (Asp) and/or glycinebetaine (GB). The results revealed that exposure to Ni caused reduced growth and membrane stability index of P. typhoideum, which were correlated with the accumulated Ni and reactive oxygen species. Oxidative stress markers; malondialdehyde, 4-hydroxy-2-nonenal and lipoxygenase were also elevated by Ni, while were diminished significantly by exogenously applied Asp and/or GB. However, considerable loss in protein and DNA contents were discernible in Ni subjected tissues, but were stimulated largely in the Asp and/or GB applied radicles. Additionally, alteration in the activities and native-PAGE profiles of antioxidant enzymes (superoxide dismutase, catalase, guaiacol peroxidase and ascorbate peroxidase) were discernible in response to Ni, which are reputed to counterbalance the oxidative condition. However, exogenous addition of Asp and/or GB activated the defense system and uplifted proline accumulation in stressed P. typhoideum. The results approved that combined addition of Asp and GB performed far better in Ni-stress mitigation than their alone application. Conducted study indicated that combined application of Asp and GB served as complementary tool to confer tolerance by up-regulating the antioxidant enzymes and thus can be implicated in the mitigation of Ni-toxicity

Salt-Responsive Metabolite, β-Hydroxybutyrate, Attenuates Hypertension

Summary: Dietary salt reduction and exercise are lifestyle modifications for salt-sensitive hypertensives. While exercise has prominent metabolic effects, salt has an adverse effect on metabolic syndrome, of which hypertension is a hallmark. We hypothesized that dietary salt impacts metabolism in a salt-sensitive model of hypertension. An untargeted metabolomic approach demonstrates lower circulating levels of the ketone body, beta-hydroxybutyrate (βOHB), in high salt-fed hypertensive rats. Despite the high salt intake, specific rescue of βOHB levels by nutritional supplementation of its precursor, 1,3-butanediol, attenuates hypertension and protects kidney function. This beneficial effect of βOHB was likely independent of gut-microbiotal and Th17-mediated effects of salt and instead facilitated by βOHB inhibiting the renal Nlrp3 inflammasome. The juxtaposed effects of dietary salt and exercise on salt-sensitive hypertension, which decrease and increase βOHB respectively, indicate that nutritional supplementation of a precursor of βOHB provides a similar benefit to salt-sensitive hypertension as exercise. : Chakraborty et al. report a link between dietary salt, a ketone, and experimental hypertension. Intake of a high salt diet lowers the ketone body beta-hydroxybutyrate (βOHB), produced by the liver, which functions to prevent Nlrp3-mediated kidney inflammation. Rescuing βOHB by nutritional supplementation of its precursor attenuates hypertension. Keywords: hypertension, metabolomics, ketone body, salt, blood pressure, β-hydroxybutyrate, inflammation, Nlrp3, inflammasome, kidne