Effect of Annona senegalensis rootbark extracts on Naja nigricotlis nigricotlis venom in rats.

Annona senegalensis Pers (family: Annonaceae) is used traditionally in Nigeria to treat victims of snakebite. The potency of the methanol extract of the root bark of the plant was tested against cobra (Naja nigricotlis nigricotlis Wetch) venom in rats. The extract was also tested on brine shrimp (Artemia saline Leach). The activity of the extract against the venom induced mortality, occurrence of toxic signs, activity on liver enzymes as well as its ability to reverse experimentally induced increase in body temperature were evaluated. Results indicated that the extract caused reduction in the induced hyperthermia and directly detoxified the snake venom used by 16-33%. It, however, failed to restore the biochemical functions (sGOT and sGPT) of the liver. The extract exhibited an LC(50) of 232.7 microg/ml in the brine shrimp test.

Is Berlina grandiflora (Leguminosae) toxic in rats?

The toxicity profile of the aqueous methanolic extract of Berlina grandiflora (BG) stem bark was studied in rats. The rats were administered graded doses (125-500 mg/kg p.o) of the extract daily for 21 days and the effects on body weight, organ weight, clinical signs, gross pathology, hematology, histology and serum biochemical parameters were measured. The relative weights of the heart, liver, kidneys and lungs of treated rats were unaffected but there were significant changes in the relative weights of the spleen and testes. The packed cell volume and hemoglobin concentrations were slightly reduced whereas total leucocytes counts were increased remarkably. Alkaline phosphatase and Creatine Kinase levels were reduced in all the groups but Glutamate oxaloacetate was significantly elevated. Total proteins and albumin levels remained normal. BG elicited a significant increase in gamma glutamyl transferase concentrations at 250 mg/kg. No significant changes occurred in urea, uric acid and BUN concentrations but calcium levels shot up remarkably. Histological findings did not reveal any treatment-related effects. The acute toxicity LD50 was estimated to be >2000 mg/kg but dose-related mortality rates of 16.7, 33.4 and 50% were observed during the sub-acute toxicity studies. These findings have once more highlighted the limitations of acute toxicity LD50 testing and suggest that BG may exert varied toxicological effects when administered orally in rats.

Investigation into the nephrotoxicity of Nigerian bonny light crude oil in albino rats.

The effect of bonny-light crude oil was assessed in adult albino rats. The rats were administered with 200, 400, and 800 mg/kg body weight of the crude oil orally for 7 days. Fluid intake was measured daily, initial and final animal body was recorded. The toxic effects on the kidneys were assessed and histological studies carried out. The results revealed that the kidney cells were damaged; crude oil caused a destruction of the renal reserve capacity. There was a significant increase (p ? 0.05) in creatinine in the high dose group (800mg/kg), and a significant decrease (p ? 0.05) in urea concentration. Histological examination indicates that crude oil induced severe pathologic changes in the forms of necrosis and oedema.

Zinc protection of mercury-induced hepatic toxicity in mice.

The actions and interactions of heavy metals on certain organ functions have been of concern, since occupational exposure to certain metals results in impairment of functions. Studies were carried out to determine the effects of zinc (Zn) and mercury (Hg) on murine liver. CD-1 male mice were administered 4 ppm HgCl2, 800 ppm ZnCl2, 4 ppm HgCl2+800 ppm ZnCl2 or deionized water in their drinking water for 12 weeks. Histological evaluation of the liver confirmed the toxic effects of Hg, as well as the normal morphology of the Zn-exposed animals. A combined treatment of both metals resulted in protection of the Hg-induced liver damage by Zn. The results of this experiment indicate that Hg has a toxic effect on liver, while Zn has a protective action against such toxic effects.