The palliative effect of camel milk on hepatic CYP1A1 gene expression and DNA damage induced by fenpropathrin oral intoxication in male rats

Autor: Gihan G. Moustafa, Abeer M. Anwer, Nabela I. El Sharkawy, Ehsan H. Abu Zeid, Ahmed G. Al Nady
Rok vydání: 2021
Předmět:
Male
Health
Toxicology and Mutagenesis
0211 other engineering and technologies
Hepatic CYP1A1
Gene Expression
02 engineering and technology
010501 environmental sciences
medicine.disease_cause
01 natural sciences
Environmental pollution
Rats
Sprague-Dawley
chemistry.chemical_compound
Malondialdehyde
Pyrethrins
GE1-350
Whole blood
Alkaline comet assay
biology
Chemistry
General Medicine
Catalase
Glutathione
Pollution
Milk
TD172-193.5
Liver
Camel milk
Environmental Pollutants
medicine.medical_specialty
Camelus
Superoxide dismutase
Internal medicine
Cytochrome P-450 CYP1A1
medicine
Animals
0105 earth and related environmental sciences
021110 strategic
defence & security studies
Superoxide Dismutase
Public Health
Environmental and Occupational Health
Rats
Environmental sciences
Comet assay
Oxidative Stress
Endocrinology
Fenpropathrin
biology.protein
Corn oil
Oxidative stress
DNA Damage
Zdroj: Ecotoxicology and Environmental Safety, Vol 207, Iss, Pp 111296-(2021)
ISSN: 0147-6513
DOI: 10.1016/j.ecoenv.2020.111296
Popis: The present study investigated the alleviating role of camel milk (CM) in the mitigation of fenpropathrin (FNP) type II pyrethroid induced oxidative stress, alterations of hepatic (CYP1A1) mRNA expression pattern, and DNA damage using the alkaline comet assay (SCGE) in male rats. Sixty male Sprague-Dawley rats were separated into six groups (n = 10): 1st control (C), 2nd corn oil (CO), 3rd (CM): gavaged CM 2ml/rat, 4th (FNP): gavaged FNP 7.09 mg/kg body weight (BW), 5th (FNP pro/co-treated): gavaged CM firstly for 15 days, then CM + FNP by the same mentioned doses and route, 6th (FNP + CM co-treated): gavaged FNP firstly followed by CM by the same mentioned doses and route. Rats were orally gavaged three times per week, day after day for 60 days. FNP exposure significantly reduced serum glutathione (GSH) levels, but significantly increased serum levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), protein carbonyl (PCO), and 8hydroxy2deoxyguanosine (8OH2dG). Additionally, FNP exposure significantly up-regulated the mRNA expression levels of hepatic CYP1A1 and increased the SCGE indices in whole blood, liver, and spleen tissues of exposed male rats. Administration of CM significantly regulated the FNP induced oxidative stress, reduced hepatic CYP1A1 mRNA expression levels and values of comet assay indices particularly in the (CM + FNP pro/co-treated) group compared to the (FNP + CM co-treated) group. In conclusion, our results indicate, for the first time, that FNP retains an in vivo genotoxic potential at a dose of (1/10 LD50) and up-regulated hepatic CYP1A1 mRNA expression in male rats. Additionally, CM supplements may improve the genotoxic outcomes, oxidative stress, and altered CYP1A1 mRNA expression induced by FNP particularly in the pro/concurrent-treatment compared to the concurrent treatment alone.
Databáze: OpenAIRE
Externí odkaz: