Sources of Human Overexposure to Fluoride, Its Toxicities, and their Amelioration Using Natural Antioxidants

Fluoride (F) is released into the environment through a combination of natural and anthropogenic processes include the weathering from volcanoes, geothermal activity, and marine aerosols. Chronic fluoride exposure has been linked with amyriad of human diseases such as skeletal and dental fluorosis, diabetes, atherosclerosis, cardiovascular diseases, and hyperkeratosis. Since fluoride targets ubiquitous enzyme reactions, it affects nearly all organ systems in animals and humans. Apart from synthetic chemical chelators, studies have been carried out to explore natural antioxidants against F toxicity. Natural products contain substances that inhibit the theoxidation of substrate(s). Antioxidant molecules are thought to play a crucial role in counteracting free-radical-induced damage to macromolecules. In this book chapter literature survey of the different phytoremediation strategy is presented. The results show that natural antioxidants exhibit promising antidote against fluoride-induced toxicity in different mammal systems

Tea Is an Elixer of Life

Green tea is a commonly consumed beverage in the world and it is a rich source of polyphenolic compounds, which are known as the tea flavonoids. Polyphenolic compounds are effective against oxidative damage in various pathological conditions. Many herbal medicines are used in traditional medicine for their protective and therapeutic properties against various diseases. Among their bioactive components, tea catechins have been found to be active against all kind of diseases including cancer. Extensive report is available that green tea displays a wide range of healthy properties, such as antioxidative, anti-inflammatory, anti-apoptotic and chemopreventors against reactive oxygen and nitrogen species. This review aims to critically analyze the available literature regarding the effects of green tea or tea catechins with special emphasis on its phytoremediation against various health disorders elicited by different chemical compounds. Overall, data in literature show tea catechins appear to be a promising elixir to recover the illness of human beings

A mechanism underlying the neurotoxicity induced by sodium fluoride and its reversal by epigallocatechin gallate in the rat hippocampus: involvement of NrF2/Keap-1 signaling pathway

Abstract Background Fluoride (Fl) exposure engenders neurodegeneration and induces oxidative stress in the brain. Therefore, the mechanism of Fl-induced neurotoxic effects needs to be determined. The aim of this study was to investigate the neuroprotective effects of EGCG (40 mg/kg) on Fl (25 mg/kg/bw)-induced oxidative stress mediated neurotoxicity with special emphasis on the hippocampus (4 weeks). Results Fl-intoxicated rat shows an increased Fl concentration along with the decreased neurotransmitter (AChE, NP, DA and 5-HT) activity in the brain. The oxidative stress markers (ROS, TBARS, NO, and PC) was significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and nonenzymatic antioxidants (GSH, TSH, and Vit.C) in the rat hippocampus. Moreover, results showed that increases in intrinsic and extrinsic apoptotic pathway leading to DNA damage and cell death were also proved by the immunohistochemical, histological, and ultra-structural studies in the Fl-treated rat hippocampus. In this context, pre-administration of EGCG significantly improved the oxidative stress, biochemical changes, cellular apoptotic and histological alternations by Fl in the hippocampus of rats. Conclusions These results confirmed the EGCG supplementation might attenuate the Fl-induced neurotoxicity via Nrf2/Keap1 signaling pathway in the rat hippocampus

Emerging promise of sulforaphane-mediated Nrf2 signaling cascade against neurological disorders

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Cholinesterase Inhibitors for Alzheimer Disease: Multitargeting Strategy based on Anti-Alzheimer's Drugs Repositioning

International audienceIn the brain, acetylcholine (ACh) is regarded as one of the major neurotransmitters. During the advancement of Alzheimer's disease (AD) cholinergic deficits occur and this can lead to extensive cognitive dysfunction and decline. Acetylcholinesterase (AChE) remains a highly feasible target for the symptomatic improvement of AD. Acetylcholinesterase (AChE) remains a highly viable target for the symptomatic improvementin AD because cholinergic deficit is a consistent and early finding in AD. The treatment approach of inhibitingperipheral AChE for myasthenia gravis had effectively proven that AChE inhibition was a reachable therapeutictarget. Subsequently tacrine, donepezil, rivastigmine, and galantamine were developed and approved for thesymptomatic treatment of AD. Since then, multiple cholinesterase inhibitors (ChEIs) have been continued to bedeveloped. These include newer ChEIs, naturally derived ChEIs, hybrids, and synthetic analogues. In this paper,we summarize the different types of ChEIs which are under development and their respective mechanisms ofactions