Sodium metaarsenite

Arsenic, a toxic metalloid, predominantly exists in soil as inorganic arsenate (As^V) and arsenite (As^III). Upon root uptake, As^V is extensively reduced to As^III in the plant. The Arabidopsis root system comprises primary, lateral and adventitious roots. It is unclear whether the inorganic arsenic-form and concentration affect specific components of the Arabidopsis root system. Synergistic and antagonistic interactions of brassinosteroids and jasmonates regulate plant development under stress, as shown by treatments with epibrassinolide (eBL) or methyl jasmonate (MeJA). However, the role of these phytohormones in root response to inorganic arsenic has been poorly studied. This research aimed to determine whether Arabidopsis roots of different type respond similarly or differently to As^III and As^V, administered as NaAsO₂ and Na₂HAsO₄·7 H₂O respectively, and whether these responses are modulated by the application of eBL and/or MeJA. The results demonstrated that As^III inhibited primary root elongation, in contrast to As^V, but promoted lateral and adventitious root formation, especially when combined with eBL. As^III, more than As^V, induced irregular cell divisions in the quiescent center and the stem cell niche of root apices, mainly of lateral roots. The As^III negative impact on lateral/adventitious roots was counteracted by eBL which favoured root formation. Xylogenesis was induced by periclinal divisions in the pericycle of the basal hypocotyl and was promoted by MeJA as a mechanical defense barrier against As^V. Collectively, results suggest that Arabidopsis responds to As by strengthening its root system and applications of eBL and MeJA ameliorate root development in specific ways, depending on the As-form.

This study examined the potential of vanillic acid (VA) to protect against renal oxidative stress and inflammation caused by sodium arsenite (SA) in mice. Mice were assigned to five groups: control, VA (100 mg/kg), SA (50 ppm in drinking water for 8 weeks), and SA + VA (50 and 100 mg/kg orally in the 7th and 8th weeks). After the experiment was ended, the Mice were sacrificed and serum and renal tissue samples were collected for additional assessments. Treatment with VA suppressed SA-induced increase in blood urea nitrogen and creatinine in the serum. Furthermore, renal histological damage induced by SA administration was ameliorated with VA treatment. Also, the increase in the level of lipid peroxidation marker (thiobarbituric acid reactive substances) along with the reduction in total thiol levels and the diminished activities of antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in the renal tissue of SA-treated mice were effectively reversed following treatment with VA. The results exhibited that the VA-treated groups (50 and 100 mg/kg) mitigated the elevation of inflammatory markers in kidney tissue (tumor necrosis factor-α and nitric oxide) in SA-exposed mice. Our research findings indicate that VA could be a potential therapeutic agent for the management of SA-associated nephrotoxicity.