Elevated, sustained, and yet reversible biotoxicity effects of lead on cessation of exposure: Melatonin is a potent therapeutic option.

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 = 10), which included control ((vehicle (normal saline) - treated) - 0.1 ml/day); lead chloride (PbCl2) untreated (3 weeks vehicle + 3 weeks Pb); Pb recovery (3 weeks Pb + 3 weeks vehicle); Pb + Mel (3 weeks Pb + 3 weeks Mel); and Mel (3 weeks vehicle + 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 malondialdehyde (MDA). Although the adverse effects of Pb on TB, ALP, AST, SOD, MDA, and TAC were sustained 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.

Investigation of the effects of dietary modification in experimental obesity: low dose of virgin coconut oil has a potent therapeutic value.

There is no report in literature on possible physiological changes that accompany dietary modification in obese condition. Moreover, there is no conclusive evidence on the optimal amount of virgin coconut oil (VCO) that could be of health benefit, although it is known to enhance lipid metabolism. Therefore, we investigated the antiobesitogenic action of graded doses of VCO (200, 400 and 600 mg/kg) in obese rats fed with normo/hyper-lipidaemic diet. Sixty rats (n = 10) were divided into 6 groups and treated as follows: the control and high fat diet (HFD) groups were administered normal saline (0.1 mL/day, p.o.) during the last four weeks of the study, and were fed with normal and HFD respectively throughout the twenty weeks duration of the experiment. Groups 3-6 were fed with HFD for 16 weeks, then normal diet during the next 4 weeks. While group - 3 received saline (0.1 mL/day, p.o.) during the last four weeks, groups 4-6 received graded doses of VCO. The results showed that HFD-induced obesity caused impaired glucose homeostasis, distorted hepatic histoarchitecture, selected deviations in hepatic function indices, pro-inflammatory, pro-oxidant, and dsylipidaemic effects. There were evidence of escalated and reversed pathological actions following the replacement of HFD with normal diet. VCO showed no effect on glucose, insulin, insulin resistance, total protein, uric acid and TAC; but equitable effects on CAT, IL-6, CRP, ALT, AST & GGT, irrespective of the dose. Compared to the effects of VCO at 400 and 600 mg/kg, at 200 mg/kg, VCO had more significant therapeutic effects on LDH, MDA, SOD, GPX, TC, TG, LDL-C, total bilirubin, atherogenic and lee indices and hepatic histoarchitecture. Conclusively, VCO, preferably at a low dose could be used to reverse hepatic structural alteration and some biochemical deviations following dietary modifications in obese condition.

Co-administration of omega-3 fatty acids and metformin showed more desirable effects than the single therapy on indices of bone mineralisation but not gluco-regulatory and antioxidant markers in diabetic rats.

Although metformin (Met) is the most recommended anti-diabetogenic drug in type 2 diabetic state, the drug is known to compromise bone integrity. Like metformin, omega-3 fatty acids (ω-3) have gluco-regulatory action; however, it aids bone health. Therefore, the present study investigated the effects of ω-3 and/or metformin in diabetic rats. Fifty rats of ten animals per group were divided into the following: Control; Diabetic untreated; Diabetic + ω-3; Diabetic + metformin (metfm) and Diabetic + ω-3 + metf groups. Diabetes was induced by the administration of streptozotocin (65 mg/kg b.w., i.p.), 15 min after the administration of nicotinamide (110 mg/kg b.w., i.p.). Five days afterwards, treatments started and they lasted for 28 days. ω-3 and metformin were administered at 200 and 180 mg/kg b.w., p.o. respectively. The results showed that the induced diabetes was characterised by significant increases in calcium to phosphorus ratio, tartrate resistant acid phosphatase (TRAP), glucose and insulin resistance; but significant decreases in parathyroid hormone(PTH), phosphorus, TAC and hepatic glycogen. Relative to the diabetic control, treatments with ω-3 or metformin caused significant elevations in hepatic glycogen, total alkaline phosphatase (TALP), osteocalcin, PTH, estradiol, and calcium; however, significant decreases in TRAP and glucose. Co-administration of ω-3 and metformin caused more desirable effects on TALP, c-terminal telopeptide of type 1 collagen, estradiol and calcium to phosphorus ratio compared to the single administration. Relative to ω-3, melatonin showed a more favourable effect on calcium to phosphorus ratio; however, the former proved to have more desirable actions on insulin and TAC. Hence, it was concluded that the combined but not the single administration of ω-3 and metformin could be preferably used in the management of bone health in diabetic state.