The Effects of Ascorbic Acid and Garlic on Bone Mineralization in Lead Exposed Pregnant Rats

Abstract

Background: Lead exposure during pregnancy may impair skeletal development. Oxidative stress is one of the important mechanisms for lead toxicity effects. The aim of this study was to investigate ascorbic acid and garlic effects on bone mineralization in lead exposed pregnant rats. Materials and Methods: In this experimental study, 50 pregnant Wistar rats were randomly divided into 5 groups; group (L) exposed to lead acetate, group (L+C) exposed to lead acetate and ascorbic acid (vitamin C), group (L+G) exposed to lead acetate and garlic juice, sham group treated with tap water plus 0.4 mL/L normal hydrogen chloride (HCl) and 0.5 mg/L sugar, control group without any intervention. All treatments were done during pregnancy. After birth, blood and bone lead levels were measured and then all neonates were sacrificed, and their right tibia bone processed for alizarin red and Alcian blue staining. Results: Blood lead levels in L group increased significantly in both mothers and their neonate compared to control animals. In addition, the neonates born to L group showed markedly higher lead concentrations in their bone than that of controls. In contrast, we found no significant changes in blood and bone lead levels in lead exposed neonates that received ascorbic acid and garlic. Bone formation in neonates of L group was clearly disrupted. Interestingly, both ascorbic acid and garlic treatments could apparently improve bone formation during pregnancy in lead exposed neonates. Conclusion: Ascorbic acid and garlic consumption during pregnancy may improve the deleterious effects of lead exposure on bone mineralization.

Amelioration of Lead-induced Toxicity in Blood, Liver and Kidney Tissues of Male Wistar Rats by Fermented Ofada Rice

“…In general, toxic metals such as lead have been known to increase the production of free radicals such as reactive oxygen species (ROS) and reactive nitrogen species (RNS) in biological systems. This in turn decreases the availability of antioxidant reserves needed to detoxify reactive intermediates leading to oxidative stress and subsequent cell/tissue damage (Ishiaq et al, 2011;Patra et al, 2011;Flora et al, 2012;Ebrahimzadeh-Bideskan et al, 2015). The induction of oxidative stress resulting in damage to key cellular components such as deoxyribonucleic acid (DNA), has been suggested as one of the possible mechanisms of metal-induced carcinogenicity and toxicity (Koedrith andSeo, 2011, Flora et al, 2012;Bandyopadhyay et al, 2014).…”