THE PROTECTIVE EFFECT OF COQ10, DHEA AND THEIR COMBINATION IN REDUCED EMBRYOTOXICITY AND TERATOGENICITY FOR NORFLOXACIN IN PREGNANT FEMALE RATS

This study was designed to evaluate the protective effect of CoQ10 and DHEA and their combination of norfloxacin induced embryotoxicity and teratogenicity in pregnant female rats and their fetuses. Twenty pregnant rats were divided equally into 5 groups, 4 animals each group as following: Control group (G1): 4 normal pregnant female received orally DMSO 0.5ml/animal/day from 5th - 19th day of gestation, first treated group (T1): 4 normal pregnant female received orally 400 mg/kg norfloxacin once daily, second treated group (T2): 4 normal pregnant female received orally 400 mg/kg norfloxacin once daily and after 1hours injected daily with CoQ10 200 mg/kg IP, third treated group (T3): 4 normal pregnant female received orally 400 mg/kg norfloxacin once daily and after 1hours injected daily with DHEA 25 mg/kg IP, and fourth treated group (T4): 4 normal pregnant female received orally 400 mg/kg norfloxacin once daily and after 1hours injected daily with a combination of CoQ10 200 mg/kg and DHEA 25 mg/kg IP for the same period. Norfloxacin was administered by oral gavages as a single dose. All dams were sacrificed at 20th day of gestation and their fetuses were collected and subjected to morphological and skeletal examinations. The obtained results showed that exposure to norfloxacin in pregnant female rats during gestational period from 5th -19th day demonstrated a significant increased (P≤ 0.05) is resorbed and stillbirth fetuses (dead fetuses at birth), and a significant decrease in fetal body weight, fetal body length, fetal tail length, maternal weight gain and placental weight; and also caused skeletal malformation in all cranial bone compared to the control group. It has been concluded that CoQ10 and DHEA prevented and treated morphological and skeletal anomalies in rat fetuses. Therefore, CoQ10 and DHEA are potential therapeutic antioxidant agents against fetotoxicity and teratogenicity induced by oxidative stress generated by norfloxacin intoxication.