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Start Over Author "Faisal Imam" Journal journal of biochemical and molecular toxicology
3 results on '"Faisal Imam"'

1. Alleviation of Aflatoxin B1-Induced Genomic Damage by ProanthocyanidinsviaModulation of DNA Repair

Author

Othman A. Al-Shabanah, Mohammed M. Attia, Saleh A. Bakheet, Mohammed M. Al-Harbi, Sabry M. Attia, Ali Alhoshani, Ahmed M. Alhuraishi, Faisal Imam, Sheikh F. Ahmad, Khaled A. Al-Hosaini, Naif O. Al-Harbi, and Shakir D. Al-Sharary

Subjects
0301 basic medicine, Chemoprotective agent, Aflatoxin, DNA repair, DNA damage, Health, Toxicology and Mutagenesis, Biology, Toxicology, medicine.disease_cause, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, medicine, heterocyclic compounds, Molecular Biology, technology, industry, and agriculture, food and beverages, General Medicine, Molecular biology, biological factors, Comet assay, 030104 developmental biology, DNA glycosylase, 030220 oncology & carcinogenesis, Molecular Medicine, Carcinogenesis, Oxidative stress
Abstract

In order to study the mechanisms underlying the alleviation of aflatoxin B1-induced genomic damage by proanthocyanidins (PAs), we examined the modulation of oxidative DNA damage induced by aflatoxin B1 in PAs-pretreated animals. The effects of PAs on changes in the expression of DNA damage and repair genes induced by aflatoxin B1 were also evaluated in rat marrow cells. Administration of PAs before aflatoxin B1 significantly mitigated aflatoxin B1-induced oxidative DNA damage in a dose-dependent manner. Aflatoxin B1 treatment induced significant alterations in the expression of specific DNA repair genes, and the pre-treatment of rats with PAs ameliorated the altered expression of these genes. Conclusively, PAs protect against aflatoxin B1-induced oxidative DNA damage in rats. These protective effects are attributed to the antioxidant effects of PA and enhanced DNA repair through modulation of DNA repair gene expression. Therefore, PAs are a promising chemoprotective agent for averting genotoxic risks associated with aflatoxin B1 exposure.

Published
2016
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2. Therapeutic potential of carfilzomib, an irreversible proteasome inhibitor, against acetaminophen-induced hepatotoxicity in mice

Author

Hesham M. Korashy, Mahmoud N. Nagi, Faisal Imam, Saleh G. Algfeley, Abdulrazaq Alanazi, and Khaled A. Al-Hosaini

Subjects
0301 basic medicine, Male, Health, Toxicology and Mutagenesis, Nitric Oxide Synthase Type II, Inflammation, Pharmacology, Toxicology, medicine.disease_cause, Biochemistry, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, medicine, Animals, Molecular Biology, Acetaminophen, chemistry.chemical_classification, Reactive oxygen species, General Medicine, Glutathione, Carfilzomib, Oxidative Stress, 030104 developmental biology, chemistry, Gene Expression Regulation, Liver, Cyclooxygenase 2, 030220 oncology & carcinogenesis, Proteasome inhibitor, Molecular Medicine, Tumor necrosis factor alpha, medicine.symptom, Reactive Oxygen Species, Oligopeptides, Proteasome Inhibitors, Oxidative stress, Injections, Intraperitoneal, medicine.drug
Abstract

Overdose of acetaminophen (APAP) is often associated with hepatotoxicity. Carfilzomib (CFZ) shows multiple pharmacological activities including anti-inflammatory potential. Therefore, this study was undertaken to evaluate the possible therapeutic effects of CFZ against APAP-induced hepatotoxicity. Hepatotoxicity was induced by administration of APAP (350 mg/kg, intraperitoneal). Mice were given CFZ (0.125, 0.25, or 0.5 mg/kg, intraperitoneal) 1.5 h after APAP administration. Animals were sacrificed on 6 h and blood and liver tissue samples were collected for analysis. In CFZ-post-treated group, there was significant and dose-dependent decrease in serum alanine aminotransferase levels. The level of tumor necrosis factor-α (TNF-α), reactive oxygen species, and NO decreased, whereas glutathione increased significantly by CFZ post-treatment. Upregulated mRNA expression of COX-II and iNOS were significantly downregulated by CFZ post-treatment. CFZ may exert its hepatoprotective action by alleviating inflammatory, oxidative, and nitrosative stress via inhibition of TNF-α, COX-II, and iNOS.

Published
2016

3. Alleviation of Aflatoxin B1-Induced Genomic Damage by Proanthocyanidins via Modulation of DNA Repair

Author

Saleh A, Bakheet, Ahmed M, Alhuraishi, Naif O, Al-Harbi, Khaled A, Al-Hosaini, Shakir D, Al-Sharary, Mohammed M, Attia, Ali R, Alhoshani, Othman A, Al-Shabanah, Mohammed M, Al-Harbi, Faisal, Imam, Sheikh F, Ahmad, and Sabry M, Attia

Subjects
Male, Aflatoxin B1, Micronucleus Tests, DNA Repair, Dose-Response Relationship, Drug, Poly (ADP-Ribose) Polymerase-1, Bone Marrow Cells, Antioxidants, DNA Glycosylases, Rats, Oxidative Stress, Gene Expression Regulation, Animals, Anticarcinogenic Agents, Proanthocyanidins, Comet Assay, Tumor Suppressor Protein p53, Micronuclei, Chromosome-Defective, Aspergillus flavus, DNA Damage, Signal Transduction
Abstract

In order to study the mechanisms underlying the alleviation of aflatoxin B1-induced genomic damage by proanthocyanidins (PAs), we examined the modulation of oxidative DNA damage induced by aflatoxin B1 in PAs-pretreated animals. The effects of PAs on changes in the expression of DNA damage and repair genes induced by aflatoxin B1 were also evaluated in rat marrow cells. Administration of PAs before aflatoxin B1 significantly mitigated aflatoxin B1-induced oxidative DNA damage in a dose-dependent manner. Aflatoxin B1 treatment induced significant alterations in the expression of specific DNA repair genes, and the pre-treatment of rats with PAs ameliorated the altered expression of these genes. Conclusively, PAs protect against aflatoxin B1-induced oxidative DNA damage in rats. These protective effects are attributed to the antioxidant effects of PA and enhanced DNA repair through modulation of DNA repair gene expression. Therefore, PAs are a promising chemoprotective agent for averting genotoxic risks associated with aflatoxin B1 exposure.

Published
2016

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