Epigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of rats
Authors: Shanmugam Thangapandiyan
Selvaraj Miltonprabu
Journal: Canadian Journal of Physiology and Pharmacology (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: sodium fluoride; hepatoprotective; EGCG; rats; hepatotoxicity
Affiliations: Department of Zoology, Annamalai University, Annamalainagar 608002, Tamilnadu, India.

Abstract:  Environmental exposure to sodium fluoride (NaF) compounds is a worldwide health concern. Epigallocatechin gallate (EGCG) is a green tea catechin found in a variety of green tea preparations. The intention of this study was to investigate the hepatoprotective role of EGCG in NaF-intoxicated rats. Rats were orally treated with NaF alone (25 mg·(kg body mass)(-1)·day(-1)) or plus EGCG at different doses (20, 40, and 80 mg·(kg body mass)(-1)·day(-1)) for 4 weeks. Hepatotoxicity of NaF was determined by increased levels of serum hepatospecific markers and total bilirubin, along with increased levels of thiobarbituric acid reactive substances, lipid hydroperoxides, protein carbonyl content, and conjugated dienes. The hepatotoxic nature of NaF was further evidenced by the decreased activity of enzymatic and nonenzymatic antioxidant levels in liver. NaF-treated rats also showed increased DNA damage and fragmentation in hepatocytes. Administration of EGCG (40 mg·(kg body mass)(-1)) to NaF-intoxicated rats significantly recuperated the distorted biochemical indices, DNA damage, and pathological changes in the liver tissue. Thus, the results of the present study clearly demonstrate that EGCG has strong free radical scavenging, antioxidant, and antigenotoxic properties that protect against NaF-induced oxidative hepatic injury in rats. 

Retracted: Yes

PubPeer comments:
 Concern about Figure 5. In Panels C and E, repetitive features appear to be visible. Could the authors please explain what happened here? This is very unexpected in biological tissues. ![file] , 
  oral supplementation of EGCG effectively protects the rat liver in multiple ways from NaF induced oxidative hepatotoxicity, when compared with the standard drug silymarin. Is silymarin **really** the standard drug for treating hepatotoxicity, whether or not induced by NaF? There are many studies in vitro and in mice, often finishing with phrases like  promising indications and  warranting further research , but I am not aware of any prescription guidelines that specify silymarin. , 
 Several panels in Fig 5 include a strip of mirror-reflected pixels down the right-hand edge, producing a kind of totem-pole effect. There is nothing particularly wrong with this artefact but it is curious. I have only seen it in papers by these authors. Do they have any idea about where in their experimental set-up it arises? ![file] ![file] , 
 Fig 4.  Effect of epigallocatechin gallate (EGCG) on DNA fragmentation in hepatocytes of control and NaF-intoxicated male albino Wistar rats. Lane 1, control (normal DNA); lane 2, EGCG treated (40 mgu00b7(kg body mass)u22121) (normal DNA); lane 3, NaF treated (25 mgu00b7(kg body mass)u22121) (severe DNA fragmentation); lane 4, NaF (25 mgu00b7(kg body mass)u22121) + EGCG (40 mgu00b7(kg body mass)u22121) treatment (mild DNA fragmentation); and lane 5, NaF (25 mgu00b7(kg body mass)u22121) + silymarin (25 mgu00b7(kg body mass)u22121) treatment (mild DNA fragmentation). Severe DNA fragmentation in lane 3 includes what appears to be a repeated section. Emphasised at right with higher contrast. ![file] , 
 2020 retraction. https: www.nrcresearchpress.com doi 10.1139 cjpp-2020-0072#.XmDLifn7TIU The Editors-in-Chief of the Canadian Journal of Physiology and Pharmacology were alerted to cases of image manipulation in the article entitled u201cEpigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of ratsu201d (see http: dx.doi.org 10.1139 cjpp-2012-0347 Thus, the Editors-in-Chief have retracted the paper from the Canadian Journal of Physiology and Pharmacology. This decision is in compliance with the publishing policy of the Canadian Journal of Physiology and Pharmacology and its publisher, Canadian Science Publishing. ,