Neurotoxic effect of lead on rats: Relationship to Apoptosis
Abstract
Background: Lead toxicity has been subjected to intensive research work, but some aspects of its mechanism needs to be elucidated.
Objectives: In the current study we aim to investigate the impact of lead toxicity on some different intermediates of apoptotic signaling pathway in experimental rats.
Design and methods: We measured caspase-8 and caspase-9 [by chemilumenescence], Bax and Bcl-2 [by ELISA] in Experimental rats, injected intraperitoneally with lead acetate for 7days at the dosage of 25, 50 and l00 mg/kg body weight and compared to control rats injected with deionized distilled water instead.
Results: Â Lead acetate significantly increased the levels of caspase 8, caspase 9 and Bax in liver, kidney and brain of experimental animals especially those with high doses. Meanwhile, caspase 8 and Bax significantly increased in brain tissue at low dose of lead, while Bcl-2 significantly increased only with advanced toxicity. Furthermore, Bax/ bcl2 ratio was significantly high in kidney (p<0.05), liver (p<0.01) and brain (p<0.01) at higher doses of lead toxicity. However, brain tissues showed significant Bax/Bcl2 ratio (p<0.05) at low lead dose. A significant positive correlation was noticed between the blood level of lead and enzymatic level of caspase 8, caspase 9 and Bax in different tissues.
Conclusion: we concluded that lead might have toxic effect through intrinsic and extrinsic induction of apoptotic pathway with prominent effect on brain tissue even at low dose.
Keywords: Lead toxicity, Rats, Apoptosis, Bcl-2, Bax, Caspase 8 and Caspase 9.
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).