Affiliation:
1. Department of Zoology, School of Basic Science SRM University Gangtok Sikkim India
2. Department of Zoology Bharathiar University Coimbatore Tamilnadu India
3. Department of Zoology University of Madras, Guindy Campus Chennai Tamilnadu India
4. Molecular Proteomics Lab Bharathiar University Coimbatore Tamilnadu India
5. Department of Zoology Cotton University Guwahati Assam India
Abstract
AbstractArsenic (As) toxicity can generate reactive free radicals, which play an important role in the evolution of cardiomyopathy. The aim of this research is to see if sulforaphane (SFN) protects against As‐induced heart damage, oxidative stress, and mitochondrial complex dysfunction via the PI3K/Akt/Nrf2 signaling pathway. The rats were placed into four groups, each with eight rats. Group 1: Normal rats (control group); Group 2: Treatment group (5 mg/kg body weight); Group 3: SFN+As‐treatment group (80 mg/kg body weight + 5 mg/kg body weight); Group 4: SFN group only (80 mg/kg body weight). The swot will last 4 weeks. At the end of the intermission (28 days), all of the rats starved overnight and killed with cervical decapitation. As administration considerably (p < 0.05) inflated the extent of free radicals (O2–, OH–), lipoid peroxidation (malondialdehyde, 4‐hydroxynonenal), lipoid profile (low‐density lipoprotein‐cholesterol, very low‐density lipoprotein‐cholesterol (VLDL‐C), total cholesterol, triglyceride, and phospholipids), cardiac Troponin (cTnT&I), and Mitochondrial complex III. A noteworthy (p < 0.05) diminish the level of HDL‐C, Mitochondrial complex I and II, enzymatic (superoxide dismutase, catalase, and glutathione peroxidase), and nonenzymatic antioxidant (glutathione and total sulfhydryl groups) and PI3k, Akt, and Nrf2 sequence in As treated rats. The western blot, real‐time polymerase chain reaction, flowcytometric, and histology studies all corroborated the biochemical findings which revealed significant heart damage in rats. Pretreatment with SFN significantly (p < 0.05) reduced the invitro free radicals, lipid oxidative indicators, mitochondrial complex, lipid profiles, and increased phase II antioxidants in the heart. This result shows that dietary supplementation of SFN protects against As‐induced cardiotoxicity via PI3k/Akt/Nrf2 pathway in rats.
Funder
Science and Engineering Research Board
Subject
Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine