Perinatal lead administration alters markers of antioxidant levels and reproductive hormone function in F1 offspring of exposed Wistar rats

Objectives: This study investigated an angle of lead intoxication via maternal inorganic lead exposure during gestation and lactation, and the outcome on some physiological indices in the first (F1) generation of the exposed female Wistar rats.

Methods: It was a multi-phased study comprising of the animal acquisition, acclimatization, mating, grouping, treatment and post-treatment/terminal protocols. Treatment was per os and on alternate days, lasting from conception, evidenced by the presence of a vaginal plug, until post-lactation in the given groups. Thus, group I served as the untreated control. Groups II, III, and IV were administered 100mg/kg, 50mg/kg, and 25mg/kg lead acetate respectively throughout gestation which lasted for 21 days. Groups V, VI, and VII received same doses but this time, up to the lactation phase; lasting for 42 days. Groups VIII, IX, and X equally received same doses respectively, but this time, during lactation only. Terminal protocols were humanely carried out upon sexual maturation of the offspring. Blood lead levels were ascertained using Varian AA240 Atomic Absorption Spectrophometer (AAS). The reproductive hormones - oestradiol (E2), Luteinizing Hormone (LH), and Follicle Stimulating Hormone (FSH), were assayed using competitive ELISA Elabscience test kits. Serum levels of the oxidative stress markers - malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH), and superoxide dismutase (SOD) - were measured using literature-derived protocols. Data obtained was expressed as mean+/-SEM (standard error of mean). Comparative analysis among groups was done using ANOVA tool of the SPSS version 25 software. P<0.05 was considered statistically significant.

RESULTS: There was a statistically significant decrease between the BLL (ppm) of the control animals in contrast to the rest of the groups. For the reproductive hormone findings, the F1 progeny of the 100mg/kg treated rats in groups II and V showed markedly reduced serum oestradiol and FSH concentrations in comparison to the control animals and others in their subgroups. Also, these same animals showed statistically significant SOD and GSH decreases in comparison to the control and other groups (P<0.05 in each case).

CONCLUSION: Our findings suggest that the antioxidant and hormone profiles of the F1 offspring can result in antioxidant and reproductive dysfunction especially in the in utero cum lactationally lead-exposed 100mg/kg treated groups. This suggests a dose-dependent response pattern as well as an oxidative stress-mediated distortion of the two key hormones affected - oestradiol and FSH.