Allium sativum Essential Oil Supplementation Reverses the Hepatic Inflammation, Genotoxicity and Apoptotic Effects in Swiss Albino Mice Intoxicated with the Lead Nitrate

Prolonged lead (Pb) exposure impairs human health due to its interference with physiological and biochemical processes. Therefore, it is necessary to investigate natural therapeutics to alleviate Pb-induced intoxication. In the current investigation, essential oil extracted from the fresh bulbs of Allium sativum was considered as a natural remedy. Initially, in vitro antioxidant and anti-inflammatory activity of A. sativum essential oil (ASEO) were explored. The results reported that ASEO exhibits potent antioxidant and anti-inflammatory potential. Additionally, an in vivo study was conducted to elucidate its preventive role against Lead-nitrate (LN)–induced hepatic damage in Swiss albino mice. The experimental mice were allocated into six groups: Control, LN-intoxicated group (50 mg/kg), LN + ASEO (50 mg/kg), LN + ASEO (80 mg/kg), LN + Silymarin (25 mg/kg), and LN + vehicle oil control group. The entire duration of the study was of 30 days. From the results, it was determined that LN exposure elevated the Pb content in hepatic tissues which subsequently increased the serum biomarkers, inflammatory cytokines (NF-kB, TNF-α, IL-6) as well as apoptotic factors (caspase-3, BAX), all of which contribute to DNA damage. Meanwhile, it reduced anti-inflammatory (IFN-γ and IL-10) and anti-apoptotic factors (Bcl-2). Furthermore, Pb accumulation in hepatic tissues changed the histological architecture, which was linked to necrosis, central vein dilation, inflammatory cell infiltration and Kupffer cell activation. In contrast to this, ASEO administration decreased the Pb content, which in turn reduced the level of serum biomarkers, inflammatory and apoptotic factors. At the same time, it increased the anti-inflammatory and anti-apoptotic factors, thereby reduced DNA damage and restored the hepatic histology. In conclusion, exhaustive research is of the utmost demand to elucidate the precise defense mechanisms of ASEO against LN-induced hepatotoxicity.