Alchornea laxiflora (Benth.) Pax & K. Hoffman extract protects against lead-induced neurodegeneration in cockerel chickens

Abstract

Lead (Pb) is a ubiquitous, non-biodegradable heavy metal contaminant with a significant impact on both human and animal health. The adverse effect of lead on health and productivity of avian species has received little attention. Alchornea laxiflora (Benth) belongs to Euphorbiaceae family and grows naturally in the Nigerian rain forest. Decoction of the leaves is usually administered traditionally to treat inflammatory and infectious diseases. The ethanol extract of Alchornea laxiflora (EaAL) leaves was used in this study to ameliorate lead-induced neurodegeneration.Seven groups of 5-week-old cockerels (n=5) were treated for 6 weeks thus: Group A - Control (water only), Group B - (100 mg/kg of EaAL daily), Group C - (200 mg/kg of EaAL daily, p.o.), Group D - (1 % lead acetate in drinking water), Group E - (1 % lead acetate in drinking water and 100 mg/kg of EaAL daily), Group F - (1 % lead acetate and 200 mg/kg of EaAL daily), Group G - (1 % lead acetate and 100 mg/kg of Vitamin C). All administrations were per os birds were euthanized on day 43 by quick cervical dislocation. Histological stains (H&E and Nissl) and Black Gold II (BGII) histochemistry were used to assess alterations in the cerebrum and cerebellum.Administration of EaAL at the two concentrations resulted in a drastic reduction in the incidence of neuropathologies observed (e.g. pyknosis and multilayering of Purkinje cells, neuronal degeneration in hippocampus cerebrum and ependymal cells, distortion of meningeal epithelial cells, etc). BGII histochemistry revealed severe demyelination caused by the administration of lead acetate, while the two doses of EaAL showed significant restoration of myelin in the cerebellum. The amelioration of demyelination observed with the use of vitamin C was considerably lower than that recorded with the use of EaAL.The use of EaAL significantly ameliorated morphological alterations and demyelination caused by the administration of lead acetate, however, caution should be exercised in the administration, as individual species idiosyncrasies may arise and the tendency to pro-oxidation at 200 mg/kg when administered alone was observed in one subject.