Search

Mohammed YI Al-Hamadani,1 Abdullah M Alzahrani,2 Mokhtar I Yousef,3 Maher A Kamel,4 Wael M El-Sayed1 1Department of Zoology Faculty of Science, Ain Shams University, Cairo 11566, Egypt; 2Department of Biological Sciences, King Faisal University, Ahsaa, Saudi Arabia; 3Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, Alexandria, Egypt; 4Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, EgyptCorrespondence: Wael M El-Sayed Tel +202/2482-1633Fax +202/2684-2123Email wael_farag@sci.asu.edu.egBackground and Aim: With the wide applications of chitosan and gold nanoparticles in drug delivery and many consumer products, there is limited available information about their effects on drug-metabolizing enzymes (DMEs). Changes in DMEs could result in serious drug interactions. Therefore, this study aimed to investigate the effects of exposure to chitosan or gold nanoparticles on hepatic Phase I and II DMEs, liver function and integrity, oxidative damage and liver architecture in male rats.Methods: Animals were divided into three equal groups: a control group, a group treated with chitosan nanoparticles (200 mg/kg, 50± 5 nm) and a group treated with gold nanoparticles (4 mg/kg, 15± 5 nm). Rats were orally administered their respective doses daily for 10 days.Results: Both chitosan and gold nanoparticles decreased the body weights by more than 10%. Gold nanoparticles reduced the activities of antioxidants (superoxide dismutase and catalase), and reduced glutathione level and elevated the malondialdehyde level in the liver. Gold nanoparticles caused significant reductions in CYP1A1, CYP2E1, quinone oxidoreductase1, and glutathione S-transferase and elevated CYP2D6 and N-acetyl transferase2. Chitosan elevated CYP2E1 and CYP2D6 and reduced UDP-glucuronosyltransferase 1A1. Both nanoparticles disturbed the architecture of the liver, but the deleterious effects after gold nanoparticles treatment were more prominent.Conclusion: Taken together, gold nanoparticles severely perturbed the DMEs and would result in serious interactions with many drugs, herbs, and foods.Keywords: CYP450, chitosan, drug interactions, drug metabolizing enzymes, oxidative stress

Propolis, a natural product derived from plant resins collected by honeybees, has been used for thousands of years in traditional medicine all over the world. Its components are strong antioxidants and free radical scavengers. On the other hand, aflatoxin B1 (AFB1) is the most potent pulmonary and hepatic carcinogen. Since the eradication of AFB1 contamination in agricultural products has been difficult, the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. The biological effects of propolis are known, but its interaction with AFB1 is not known for therapeutic uses. Therefore, this study was designed to examine the protective effects of different concentrations of propolis (6.25, 12.5, 25, 50 and 100 mg/L) against AFB1 (3.12 ppm) genotoxicity in human lymphocytes in vitro. The genotoxic effects were assessed by micronucleus (MN) test in human blood cultures. The results of the present study indicated that AFB1 significantly (P

The present study was designed to investigate genotoxic and cytotoxic effects and oxidative damage of increasing concentrations of nano-hydroxyapatite (5, 10, 20, 50, 75, 100, 150, 300, 500 and 1000 ppm) in primary human blood cell cultures. Cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay and lactate dehydrogenase release, while total antioxidant capacity and total oxidative stress levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by sister chromatid exchange, micronuclei, chromosome aberration assays and 8-oxo-2-deoxyguanosine level as indicators of genotoxicity. The results of [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] and lactate dehydrogenase assays showed that the higher concentrations (150, 300, 500 and 1000 ppm) of hydroxyapatite nanoparticles (HAP NPs) decreased cell viability. HAP NPs led to increases of total oxidative stress (300, 500 and 1000 ppm) levels and decreased total antioxidant capacity (150, 300, 500 and 1000 ppm) levels in cultured human blood cells. On the basis of increasing concentrations, HAP NPs caused significant increases of sister chromatid exchange, micronuclei, chromosome aberration rates and 8-oxo-2-deoxyguanosine levels as compared to untreated culture. In conclusion, the obtained in vitro results showed that HAP NPs had dose-dependent effects on inducing oxidative damage, genotoxicity and cytotoxicity in human blood cells.