RETRACTED: Diallyl trisulfide, a garlic polysulfide protects against As-induced renal oxidative nephrotoxicity, apoptosis and inflammation in rats by activating the Nrf2/ARE signaling pathway
Authors: S Miltonprabu
P Senthilraja
N C Sumedha
Journal: International Immunopharmacology (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Antioxidant; As; Diallyl trisulfide; Nrf2/Keap1; Rats
Affiliations: Department of Zoology, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamilnadu, India. Electronic address: ., Department of Zoology, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamilnadu, India., Division of Bioinformatics, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamilnadu, India.

Abstract:  Background: Arsenic (As) contamination is an extremely dangerous global environmental problem as it can enter into the food chain and become bio-accumulated, endangering human health. Chronic As intoxication leads to undesirable toxic effects in various organ systems of the body, especially the kidney. Diallyl trisulfide (DATS) is an organosulfur compound which has been widely known for its uses as antibacterial, antitumorogenic, antioxidant agent and has been also reported to have anti-apoptotic and anti-inflammatory properties. Purpose: In the present work, we intend to investigate the protective role of DATS, a garlic organosulfur compound in preventing the As-induced oxidative stress mediated renal injury in rats. Study design The activity of DATS to antagonize As-induced renal oxidative toxicity was analyzed using rats as an in vivo model. Methods: We investigated the nephroprotective effect of DATS on As treated rats by performing various serological, biochemical, molecular and histological studies. The activation of Nrf2 was investigated using western blot. Results: The data showed that As exposure significantly increased the serum and urine nephritic, oxidative stress, apoptosis and inflammatory markers in the renal tissue of rats. As intoxication also decreased the antioxidant status of the renal tissue along with the disturbances in the membrane bound ATPases. As nephrotoxicity was further confirmed with the altered morphological and ultrastructural changes in the renal tissue. Conversely, the DATS pre-administration effectively recuperate the altered renal variables by As, which has been further supported by the histological and ultrastructural observations. This counteraction was achieved partially via the activation of Nrf2-ARE pathway through the activation of Akt. Conclusion: These findings explicate the prospective use of DATS as a promising organosulfur compound against As-induced renal oxidative dysfunction in rats. 

Retracted: Yes

PubPeer comments:
 Concern about Figure 7. Panels A (control rats) and D (DATS alone rats) share many parts, just in a different order. In addition, some parts appear to be visible multiple times within panel D. There is also a possible repeat within panel B.  , 
 Concern about Figure 7. Panels A (control rats) and D (DATS alone rats) share many parts, just in a different order. In addition, some parts appear to be visible multiple times within panels A, C, and D.  , 
 Concern about Figure 10. In the top left panel B, the same area appears to be visible twice. Shown with blue boxes.  , 
 Concern about Figure 11, bottom panels. Repetitive features appear to be visible in all four panels.  , 
 #4 Unexpected 180-deg rotational symmetry of the nuclei of A and D. One large section is repeated between (A) and (D) apart from a 90-deg rotation.  , 
 2020 retraction notice. https: www.sciencedirect.com science article pii S1567576920316003?via%3Dihub This article has been retracted at the request of the request of the Editor-in-Chief. Portions of the photomicrographs in Figures. 7A and 8A have been duplicated. As such this article represents a misuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. We thank Dr Elisabeth Bik for drawing the irregularities to the journal s attention. ,