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Arsenic (As) is a metalloid prevalent mainly in soil and water. The presence of As above permissible levels becomes toxic and detrimental to living organisms, therefore, making it a significant global concern. Humans can absorb As through drinking polluted water and consuming As-contaminated food material grown in soil having As problems. Since human beings are mobile organisms, they can use clean uncontaminated water and food found through various channels or switch from an As-contaminated area to a clean area; but plants are sessile and obtain As along with essential minerals and water through roots that make them more susceptible to arsenic poisoning and consequent stress. Arsenic and phosphorus have many similarities in terms of their physical and chemical characteristics, and they commonly compete to cause physiological anomalies in biological systems that contribute to further stress. Initial indicators of arsenic's propensity to induce toxicity in plants are a decrease in yield and a loss in plant biomass. This is accompanied by considerable physiological alterations; including instant oxidative surge; followed by essential biomolecule oxidation. These variables ultimately result in cell permeability and an electrolyte imbalance. In addition, arsenic disturbs the nucleic acids, the transcription process, and the essential enzymes engaged with the plant system's primary metabolic pathways. To lessen As absorption by plants, a variety of mitigation strategies have been proposed which include agronomic practices, plant breeding, genetic manipulation, computer-aided modeling, biochemical techniques, and the altering of human approaches regarding consumption and pollution, and in these ways, increased awareness may be generated. These mitigation strategies will further help in ensuring good health, food security, and environmental sustainability. This article summarises the nature of the impact of arsenic on plants, the physio-biochemical mechanisms evolved to cope with As stress, and the mitigation measures that can be employed to eliminate the negative effects of As. [ABSTRACT FROM AUTHOR]

Platelet shape and volume changes are early mechanical events contributing to platelet activation and thrombosis. Here, we identify single-nucleotide polymorphisms in Leucine-Rich Repeat Containing 8 (LRRC8) protein subunits that form the Volume-Regulated Anion Channel (VRAC) which are independently associated with altered mean platelet volume. LRRC8A is required for functional VRAC in megakaryocytes (MKs) and regulates platelet volume, adhesion, and agonist-stimulated activation, aggregation, ATP secretion and calcium mobilization. MK-specific LRRC8A cKO mice have reduced arteriolar thrombus formation and prolonged arterial thrombosis without affecting bleeding times. Mechanistically, platelet LRRC8A mediates swell-induced ATP/ADP release to amplify agonist-stimulated calcium and PI3K-AKT signaling via P2X1, P2Y 1 and P2Y 12 receptors. Small-molecule LRRC8 channel inhibitors recapitulate defects observed in LRRC8A-null platelets in vitro and in vivo . These studies identify the mechanoresponsive LRRC8 channel complex as an ATP/ADP release channel in platelets which regulates platelet function and thrombosis, providing a proof-of-concept for a novel anti-thrombotic drug target.