Shanmugam Thangapandiyan1, Mathan Ramesh2, Tamilselvan Hema2, Selvaraj Miltonprabu3, Md Sahab Uddin4, Venkatesan Nandhini2, Gunasekaran Bavithra Jothi2.
Abstract
BACKGROUND/AIMS: Agriculture and industrial expansion in recent years have resulted in the undue discharge of arsenic into the environment, building arsenic toxicity a major worldwide anxiety. Oxidative stress is considered as the most conspicuous effect of arsenic toxicity. The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.
METHODS: For this purpose, male Wistar rats were randomly distributed into 6 groups of 8 rats each: control, Arsenic (5mg/kg BW), SFN plus Arsenic (20, 40, 80 mg/kg BW; 5mg/kg BW) and Vit. C plus Arsenic (100mg/kg BW; 5mg/kg BW). In this study, we have used spectrophotometry for enzymatic antioxidant assays, western blotting and PCR for protein and gene expression. Microtome for histological study.
RESULTS: The arsenic-induced oxidative damage was confirmed by a significant (p<0.05) increase in the levels of ALAD, As concentration and depletion in the antioxidant content. Furthermore, Arsenics treatments significantly (p<0.05) increased the pro-apoptotic marker (Bax) and DNA damage, with decreased Nrf2 protein responsible for liver protection. However, pretreatment with SFN significantly (p<0.05) decreased the levels of ALAD, Arsenic concentration, and brought antioxidant enzymes into normal levels. This was accomplished by inhibition of apoptotic markers via activation of PI3K, Akt and Nrf2 mediated signaling pathway as evident from western blotting and PCR techniques.
CONCLUSION: Moreover, SFN pretreatment shield the liver histoarchitecture observed in Arsenic treated groups suggesting prevention of liver toxicity via PI3K/Akt mediated Nrf2 signaling pathways and could possibly provide a protection against Arsenic induced hepatic burden. © Copyright by the Author(s). Published by Cell Physiol Biochem Press.
BACKGROUND/AIMS: Agriculture and industrial expansion in recent years have resulted in the undue discharge of arsenic into the environment, building arsenic toxicity a major worldwide anxiety. Oxidative stress is considered as the most conspicuous effect of arsenic toxicity. The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.
METHODS: For this purpose, male Wistar rats were randomly distributed into 6 groups of 8 rats each: control, Arsenic (5mg/kg BW), SFN plus Arsenic (20, 40, 80 mg/kg BW; 5mg/kg BW) and Vit. C plus Arsenic (100mg/kg BW; 5mg/kg BW). In this study, we have used spectrophotometry for enzymatic antioxidant assays, western blotting and PCR for protein and gene expression. Microtome for histological study.
RESULTS: The arsenic-induced oxidative damage was confirmed by a significant (p<0.05) increase in the levels of ALAD, As concentration and depletion in the antioxidant content. Furthermore, Arsenics treatments significantly (p<0.05) increased the pro-apoptotic marker (Bax) and DNA damage, with decreased Nrf2 protein responsible for liver protection. However, pretreatment with SFN significantly (p<0.05) decreased the levels of ALAD, Arsenic concentration, and brought antioxidant enzymes into normal levels. This was accomplished by inhibition of apoptotic markers via activation of PI3K, Akt and Nrf2 mediated signaling pathway as evident from western blotting and PCR techniques.
CONCLUSION: Moreover, SFN pretreatment shield the liver histoarchitecture observed in Arsenic treated groups suggesting prevention of liver toxicity via PI3K/Akt mediated Nrf2 signaling pathways and could possibly provide a protection against Arsenic induced hepatic burden. © Copyright by the Author(s). Published by Cell Physiol Biochem Press.
Entities:
Keywords:
Arsenic; Hepatotoxicity; Liver; Nrf2; PI3K/Akt pathway; Sulforaphane
Mesh：
Substances：
Year: 2019
PMID： 31001960 DOI： 10.33594/000000082
Source DB: PubMed Journal: Cell Physiol Biochem ISSN： 1015-8987