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

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

Epigallocatechin gallate supplementation protects against renal injury induced by fluoride intoxication in rats: Role of Nrf2/HO-1 signaling

Fluoride intoxication generates free radicals, causing oxidative stress that plays a critical role in the progression of nephropathy. In the present study, we hypothesized that epigallocatechin gallate (EGCG), found in green tea, protects the kidneys of rats treated with fluoride by preventing oxidative stress, inflammation, and apoptosis. Pretreatment of fluoride-treated rats with EGCG resulted in a significant normalization of creatinine clearance and levels of urea, uric acid, and creatinine. Fluoride intoxication significantly increased renal oxidative stress markers and decreased the levels of renal enzymatic and non-enzymatic antioxidants. In addition, renal NO, TNF-α, IL-6 and NF-κB were also increased in the renal tissue of fluoride-treated rats. Further, EGCG pretreatment produced a significant improvement in renal antioxidant status and reduced lipid peroxidation, protein carbonylation and the levels of inflammatory markers in fluoride-treated kidney. Similarly, mRNA and protein analyses showed that EGCG pretreatment normalized the renal expression of Nrf2/Keap1 and its downstream regulatory proteins in fluoride-treated rat kidney. EGCG also effectively attenuated fluoride-induced renal apoptosis by the up-regulation of anti-apoptotic proteins such as Bcl-2 and down-regulation of Bax, caspase-3, caspase-9 and cytochrome c. Histology and immunohistochemical observations of Kim-1 provided further evidence that EGCG effectively protects the kidney from fluoride-mediated oxidative damage. These results suggest that EGCG ameliorates fluoride-induced oxidative renal injury by activation of the Nrf2/HO-1 pathway

Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats. Keywords: Cd, GSP, Mitochondria, Oxidative stress, Liver, Rat

Biochemical Perturbations and Metabolic Derangements Induced by Benzophenone-3 at Environmentally Relevant Concentration in the Liver of Danio rerio

UV filters are used daily by millions of people. many wastewater treatments plants are ill-equipped to filter them properly. As a result, UV filters are progressively reaching the environment at an alarming level. Benzophenone-3(BP3) in particular, are toxic to all organisms. Its toxic effects include coral bleaching and interference with metabolic, enzymatic, and reproductive activities. The present study aims to assess the toxic impact of environmentally relevant concentration of BP3(44μg/l) on some selected biochemical variables in the liver tissue of Zebra fish on different exposure periods. The exposed fishes were shown to exhibit significant alterations in the carbohydrate, lipid and protein levels and their metabolism and elevated the level of transaminases in the hepatic tissue. The severity of derangement was slowly increased upon increasing exposure period and more significant at the 45th days of exposure. From our results, it may suggested that BP3 exposure at sub chronic periods even at the environmentally relevant concentration might induce intense biochemical alterations in the liver of D.rerio

Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis

The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats

Potential Nephrotoxic Effect of UV-328 and Its Possible Salvage by Dimethoxy Curcumin in Zebrafish

The occurrence of Benzotriazole UV Stabilizer-328 (UV-328) in different environmental and natural systems is of fast regular concern these days. In this current paper, we assessed the renotoxicity of UV-328 in zebrafish kidney tissues to know the chore of oxidative devilry in kidney and to recuperate the renotoxicity utilizing Dimethoxy curcumin (DiMC) supplementation. Grown-up zebrafish were exposed 55µg/L of UV-328 and DiMC supplemented through diet at 50mg/kg BW. Close to the completion of 28 days, renal tissues were examined for the responses of oxidative pressure, antioxidant status and histopathological changes. The results demonstrated that antioxidant enzymes such as, Glutathione (GSH) levels and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) were all reduced in zebra fish kidneys treated with UV-328. Renal malondialdehyde (MDA) levels was brought prominently up in the UV-328 treated fish. All of the altered variables significantly returned to near-normal levels in the DiMC-supplemented group. Histopathological lesions, viz., hypertrophied glomerulus, cytoplasmic and nuclear degeneration, cytoplasmic vacuolization, degeneration of renal tubules were seen in UV-328 treated kidney of zebrafish which were actually reinforced in the DiMC treated fish. From our outcomes, it has been proposed that even at the low-level convergence of UV-328 exposure is malicious and to provoke oxidative insult, cell reinforcement exhaustion and kidney neurotic devilry in zebrafish and remediation with DiMC has been ended up being the better choice to conquer the harmful oppression prompted by UV-328

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

Hepatoprotective effect of quercetin: From chemistry to medicine

Liver diseases caused by viral hepatitis infections have a negative impact on global health. Approximately 30 million people in the USA and 29 million people in the European Union suffer from chronic liver disease. There are many kinds of diseases of the liver, caused by viruses, such as hepatitis A, hepatitis B and hepatitis C, or by certain drugs and poisons including excessive alcohol consumption. Many herbal medicines are used in traditional medicine for their protective and therapeutic properties against liver diseases. Among their bioactive components, flavonoids have been found to be active against liver dysfunction and damage caused by liver diseases. Extensive evidences report that quercetin (QE), a major flavonol commonly found in apple, berries, onion, citrus fruits, cruciferous vegetables, tea, pepper, tomato, whole gain, cocoa and red wine, displays a wide range of healthy properties, including anti-oxidative, anti-inflammatory, anti-apoptotic and hepatoprotective activities against various hepatic ailments. This review aims to critically analyze the available literature regarding the hepatoprotective effects of QE with special emphasis on its mechanisms of actions. To provide a complete picture of QE, its distribution, chemistry, biosynthesis and bioavailability are reported. Overall, data in literature shows that QE appears to be a promising hepatoprotective compound

Hepatoprotective effect of quercetin: From chemistry to medicine

Liver diseases caused by viral hepatitis infections have a negative impact on global health. Approximately 30 million people in the USA and 29 million people in the European Union suffer from chronic liver disease. There are many kinds of diseases of the liver, caused by viruses, such as hepatitis A, hepatitis B and hepatitis C, or by certain drugs and poisons including excessive alcohol consumption. Many herbal medicines are used in traditional medicine for their protective and therapeutic properties against liver diseases. Among their bioactive components, flavonoids have been found to be active against liver dysfunction and damage caused by liver diseases. Extensive evidences report that quercetin (QE), a major flavonol commonly found in apple, berries, onion, citrus fruits, cruciferous vegetables, tea, pepper, tomato, whole gain, cocoa and red wine, displays a wide range of healthy properties, including anti-oxidative, anti-inflammatory, anti-apoptotic and hepatoprotective activities against various hepatic ailments. This review aims to critically analyze the available literature regarding the hepatoprotective effects of QE with special emphasis on its mechanisms of actions. To provide a complete picture of QE, its distribution, chemistry, biosynthesis and bioavailability are reported. Overall, data in literature shows that QE appears to be a promising hepatoprotective compound