Arsenic Induced Oxidative Neural-Damages in Rat are Mitigated by Tea-Leave Extract via MMPs and AChE Inactivation, Shown by Molecular Docking and in Vitro Studies with Pure Theaflavin and AChE.

Background: Chronic arsenic-exposure causes neuromuscular disorders and other health anomalies. Damage to DNA and cytoskeletal/extracellular matrix is brought on by reactive-oxygen-species (ROS)-induced intrinsic antioxidant depletion (thiols/urate). Therapeutic chelating-agents have multiple side-effects.

Different mechanisms of arsenic related signaling in cellular proliferation, apoptosis and neo-plastic transformation.

Arsenic is a toxic heavy metal vastly dispersed all over the earth crust. It manifests several major adverse health issues to millions of arsenic exposed populations. Arsenic is associated with different types of cancer, cardiovascular disorders, diabetes, hypertension and many other diseases.

Protection against Mitochondrial Oxidative-Stress by Flesh-Extract of Edible Freshwater Snail Bellamya bengalensis Prevents Arsenic Induced DNA and Tissue Damage.

Aims: Arsenic has carcinogenic properties because of the formation of Reactive Oxygen Species (ROS). ROS damages different macromolecules, tissues and organs, and severely exhausts cellular antioxidants.

Background: Cytosolic and mitochondrial contribution of ROS production by arsenic are not well reported.

Neurotoxic Mechanism of Arsenic: Synergistic Effect of Mitochondrial Instability, Oxidative Stress, and Hormonal-Neurotransmitter Impairment.

Arsenic toxicity which is now a global concern is predicted to affect more than 200 million people. Chronic arsenic exposure conduce carcinogenicity, hepatotoxicity, and neurotoxicity. Here we have reviewed numerous epidemiological and experimental reports related to arsenic toxicity to explore its neurotoxicity mechanism.