Phoenix dactylifera L. Seeds Could Alleviate the Aflatoxin B1-provoked Heart Injury in Male Offspring Rat During Transplacental and Translactational: The Impact of Inflammatory, Apoptotic Pathways, and Oxidative Stress. |
Paper ID : 1013-FCANVU |
Authors |
Hanan M.A El Henafy *1, Walaa A M Eid2 1Medical Laboratory Department, Faculty of Applied Health Sciences, October 6 University, Giza 3230911, Egypt. 22 Food Science and Technology Dept., Fac., Agric., New Valley Univers., Elkgarga City, Egypt. |
Abstract |
Aflatoxin B1 (AFB1) is an inevitable environmental hazard that pollutes foods, causing a grave threat to the health of humans and animals. Phoenix dactylifera L. Seeds(PDL) has recently evoked significant attention for their therapeutic potential as an effective therapy for numerous diseases. This study investigated potential pathways beyond the protective effect of PDL against AFB1-induced cardiotoxicity in male offspring. Forty-eight female albino rats received 200 mg/kg/day of PDL orally for 14 days before mating till weaning and 50 μg/kg/day of AFB1 intramuscularly throughout gestation and lactation. Postnatal day 60, male offspring samples were collected to evaluate oxidative stress and apoptotic markers. AFB1 induced cardiac toxicity in rats, which hypothesized to be conducted by the development of DNA damage, altering redox state, modification of gene expression, and dysregulation of cytokine production. AFB1 was elevated LDH, CK-MB,CK, 8-OHdG, MDA, NO, TNF-α, beclin-1, IL-6, IL-1β, Nrf2, IL-1, ICAM-1, and caspase-3. In addition, it significantly lowered GSH, GRD, TSSA, CAT, SOD, NSSA, GST, and GPx in offspring. RT- PCR analysis showed that AFB1 decreased Bcl2 expression and elevated caspase-3, Bax, ACE1, P53, and cytochrome C in the heart. PDL has comprised of polyphenol compounds. Antioxidant, anti-inflammatory, and free radical-trapping of polyphenols mitigated AFB1-induced cardiac toxicity and apoptosis. |
Keywords |
Keywords: Phoenix dactylifera L Aflatoxin B1; Maternal exposure; oxidative stress; Toxicity. |
Status: Accepted |