Role of copeptin as a novel biomarker of bisphenol A toxic effects on cardiac tissues: biochemical, histological, immunohistological, and genotoxic study.

Copeptin is a precursor for arginine vasopressin which is usually elevated in acute stress and cardiac emergencies. Bisphenol A (BPA) is an ideal plasticizing factor used in manufacturing of plastics and epoxy resins. To evaluate the cardio toxicity of bisphenol A and to assess copeptin as a cardio toxic diagnostic and prognostic biomarker in Wistar rats. Sixty Wistar rats were classified into three groups: group I, naive group received regular diet and water; group II, vehicle group administered corn oil; and group III, each rat received BPA daily with (30 mg/kg/day S.C). After 4 weeks, blood samples were collected for estimating serum copeptin levels. Then, the hearts were subjected to histological, immunohistochemical, and electron microscopic examination. Cell suspensions from the hearts were examined to determine the extent of DNA damage by comet assay. Bisphenol A induced a significant increase in mean values of serum copeptin level, histopathological changes in the form of dilated congested blood vessels and extensive collagen fiber deposition in the myocardium. Ultrastructurally, disturbed indented nuclei, focal lysis of myofibrils, normal cross striations loss, mitochondrial swelling, and intercalated disks distortion were noticed. Immunohistochemical study showed a significant increase in TLR2 immunoreactions in the myocytes of BPA administered rats. In addition, comet assay showed that bisphenol A exposure produced DNA damage in cardiac cells. We concluded that bisphenol A has deleterious effects on cardiac tissues mean, while copeptin is a good diagnostic and prognostic biomarker.

Protective effects of tribulus terrestris extract and angiotensin blockers on testis steroidogenesis in copper overloaded rats.

The rational of the current study was to assess whether Tribulus terrestris extract (TTE) could alleviate long-term copper (Cu) overload-induced testicular dysfunction compared to enalapril and losartan. Rats were administered either vehicle (control group, n = 10) or copper sulfate pentahydrate (CuSO4·5H2O, 200 mg/kg, p.o) for 90 days (n = 40). Cu-treated rats were randomized into four equal groups. One group was left untreated (Cu group) while the remaining three groups were daily co-treated with one of the following treatments along with CuSO4: TTE (10 mg/kg, p.o); enalapril (30 mg/kg, p.o); losartan (10 mg/kg, p.o). Excess Cu intake resulted in Cu overload coupled with a significant elevation in systolic blood pressure and serum angiotensin II levels along with a reduction in serum nitric oxide level. All concomitant treatments led to an alleviation of such deleterious effects. However, only losartan failed to ameliorate angiotensin II elevation. Additionally, all treatments protected the testes against Cu-overload-elicited zinc depletion and oxidative stress. Regarding reproductive function, the relative weights of testes, serum levels of testosterone and luteinizing hormone; the expression of steroidogenic genes; the protein levels of angiotensin II type 1 receptor and angiotensin converting enzyme 1, in addition to its activity, they were significantly reduced. Amongst all treatments, only TTE and E were able to revert these reproductive changes. In conclusion TTE and E were able to protect against Cu overload-induced impairment of testicular steroidogenesis. Thus, they might be considered as prophylactic drugs of choice against hypertension and testicular dysfunction to ameliorate Cu overload risk.