In the present study, we investigated the effect of the p-Coumaric acid (PCA), a phenolic acid, on potassium bromate (KBrO ) induced oxidative damage, Ras/Raf/MEK signaling, and apoptosis in HepG2 cells. Our findings showed that PCA-treated cells prevented cytotoxicity compared with KBrO treated cells. Furthermore, KBrO -induced oxidative stress and lipid peroxidation was attenuated by PCA and it also increased the antioxidant levels such as SOD, CAT, and GPX. Additionally, PCA inhibited the KBrO -induced DNA damage in HepG2 cells. Moreover, PCA treatment suppressed the activation of Ras/Raf/MEK signaling and increased the expression of PRDX-1. In addition, PCA prevented the KBrO -induced apoptosis cascade by altering the expression of proapoptotic, Bax, caspase-3, and antiapoptotic, Bcl-2 proteins. The present study proves that PCA inhibited the KBrO -induced oxidative stress, DNA damage, and apoptotic signaling cascade in HepG2 cells.
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http://dx.doi.org/10.1002/cbf.3837 | DOI Listing |
Nat Commun
December 2024
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT, 05405, USA.
8-oxoguanine (8-oxoG) is a common oxidative DNA lesion that causes G > T substitutions. Determinants of local and regional differences in 8-oxoG-induced mutability across genomes are currently unknown. Here, we show DNA oxidation induces G > T substitutions and insertion/deletion (INDEL) mutations in human cells and cancers.
View Article and Find Full Text PDFCell Biochem Funct
June 2024
Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, India.
Potassium bromate (KBrO) is a common dietary additive, pharmaceutical ingredient, and significant by-product of water disinfection. p-coumaric acid (PCA) is a naturally occurring nutritional polyphenolic molecule with anti-inflammatory and antioxidant activities. The goal of the current investigation was to examine the protective effects of p-coumaric acid against the liver damage caused by KBrO.
View Article and Find Full Text PDFMutat Res Genet Toxicol Environ Mutagen
March 2024
Division of Pathology, National Institute of Health Sciences, 3-25-26 Tonomachi, Kawasaki-ku, Kawasaki-shi, Kanagawa, 210-9501, Japan; Faculty of Animal Health Technology, Yamzaki University of Animal Health Technology, 4-7-2 Minamiosawa, Hachioji-shi, Tokyo, Japan. Electronic address:
Genome Res
February 2024
Department of Medical Biophysics and Radiation Biology, Faculty of Medical Sciences, Kyushu University, Fukuoka, Fukuoka 812-8582, Japan.
Oxidative stress-induced DNA damage and its repair systems are related to cancer etiology; however, the molecular basis triggering tumorigenesis is not well understood. Here, we aimed to explore the causal relationship between oxidative stress, somatic mutations in pre-tumor-initiated normal tissues, and tumor incidence in the small intestines of MUTYH-proficient and MUTYH-deficient mice. MUTYH is a base excision repair enzyme associated with human colorectal cancer.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2024
Molecular Toxicology and Biomedical Research Group, Department of Biochemistry, College of Biosciences, Federal University of Agriculture, Abeokuta, Nigeria.
This study explored the effect of naringin (NAR) on HGPRT1 deficiency and hyperuricemia through NOS-cAMP-PKA and BDNF/TrkB signaling pathways induced by caffeine (CAF) and KBrO in a rat model. Sixty-three adult male albino rats were randomly assigned into nine (n = 7) groups. Group I: control animals, Group II was treated with 100 mg/kg KBrO , Group III was treated with 250 mg/kg CAF, Group IV was treated with 100 mg/kg KBrO + 250 mg/kg CAF, Group V was administered with 100 mg/kg KBrO + 100 mg/kg haloperidol, Group VI was administered with 100 mg/kg KBrO + 50 mg/kg NAR, Group VII was administered with 500 mg/kg CAF + 50 mg/kg NAR, and Group VIII was administered with 100 mg/kg KBrO + 250 mg/kg CAF + 50 mg/kg NAR.
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