Elevated, sustained, and yet reversible biotoxicity effects of lead on cessation of exposure: Melatonin is a potent therapeutic option
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Date
2020-06-03
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Toxicology and Industrial Health
Abstract
Melatonin (Mel) is known to prevent and mitigate lead (Pb)-induced gonadotoxicity. However, there is no
report in literature on the endogenous levels of different biomarkers after the cessation of Pb exposure, with
or without treatment with Mel. Fifty adult male Wistar rats were divided into five groups (N 1⁄4 10), which
included control ((vehicle (normal saline) - treated) 0.1 ml/day); lead chloride (PbCl2) untreated (3 weeks
vehicle þ 3 weeks Pb); Pb recovery (3 weeks Pb þ 3 weeks vehicle); Pb þ Mel (3 weeks Pb þ 3 weeks Mel); and
Mel (3 weeks vehicle þ 3 weeks Mel) groups. Pb and Mel were administered at 50 and 10 mg/kg B.W. (p.o.),
respectively. The results showed that Pb caused significant decreases in total bilirubin (TB), phospholipids
(PLP), superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC), but significant
elevations in alkaline phosphatase (ALP), aspartate aminotransferase (AST), triglyceride (TG), and mal-
ondialdehyde (MDA). Although the adverse effects of Pb on TB, ALP, AST, SOD, MDA, and TAC were sus-
tained after the cessation of exposure, a reversal was observed in total cholesterol (TC), TG, PLP, CAT, and
c-reactive protein (CRP) results. Nevertheless, the detrimental effects of Pb on alanine aminotransferase
(ALT), albumin, and globulin were only expressed post-exposure. Treatment with Mel caused no significant
effect on TB and albumin levels. However, unlike TAC and CRP, the hormone significantly reduced ALP, AST,
ALT, TC, low-density lipoprotein cholesterol, PLP, SOD, CAT, MDA, and globulin to levels comparable to the
control group. In conclusion, following the cessation of Pb exposure, alterations in physiological balance could
be elevated, sustained, or reversible. However, Mel enhanced the reestablishment homeostatic status after Pb
administration.
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Lead, melatonin, hepatic, antioxidant, inflammation