Context:Zingiber officinale (Zingiberaceae) is a herb used for culinary and therapeutic purposes due to its anti-inflammatory and antioxidant potentials.Objectives:We examined its protective ability against mercury (Hg), lead (Pb) and cadmium (Cd) accumulation in the liver.Materials & Methods:Ground Zingiber officinale (7%, w/w of feed) was administered to rats either at the same time with the exposure ofheavy metals (group 2), a week after exposure to heavy metals (group 3) or given a week before heavy metal exposure (group 4) for six weeks. Animals were exposed to either of Hg (10 ppm), Cd (200 ppm) and Pb (100 ppm) in drinking water. The heavy metal accumulations in the liver were determined using AAS.Results:Weight losses induced by these metals were not reversed by Zingiber officinale administration. There was a significant (P<0.01) increase in protection to Pb (97%) and Cd (63%) accumulation when compared to Hg (32%) at week 2. The protective ability was significantly (P<0.01) decreased at week 4 when compared to week 2 for Cd and Pb but not to Hg in groups 3 (50%) and 4 (52%). At week 6, hepatoprotection to Hg (44%) and Cd (85%) was significantly (P<0.01) different but not to Pb which was only significant (P<0.05) in week 2 of treatment for all groups.Discussion and Conclusion:Zingiber officinale affected the bioavailability, elimination and uptake of these metals in a time-dependent way with highest beneficial reducing effect to Cd followed by Hg and least protection to Pb in the liver.
Apocynin is reported to have antioxidant and NADPH oxidase inhibitor activities. Cadmium toxicity is reported to causes oxidative damage, resulting in vascular dysfunction, reduced bioavailability of nitric oxide (NO) and hypertension. The study aimed to investigate the protective effects of apocynin in cadmium-induced hypertension. Thirty-six (36) adult male Sprague-Dawley rats were randomly divided into 6 groups. Group 1 served as control, Groups 2 and 3 received 50 and 100 mg/Kg (b.w) apocynin, respectively, Group 4 received 100 ppm CdCl2 in their drinking water, while Group 5 and 6 received 100 ppm CdCl2 in their drinking and 50 and 100 mg/Kg (b.w) apocynin, respectively, for 8 weeks. Blood pressure readings were taken weekly using the tail-cuff method. cGMP, endothelial nitric oxide synthase (eNOS), NO and hematological parameters were analyzed at the end of 8 weeks. Apocynin, although a poor antioxidant, caused a significant reduction (p < 0.05) in systolic and mean arterial pressures in the cadmium-induced elevations in blood pressure and amelioration of altered hematological parameters. However, while cadmium exposures did not alter the cGMP, eNOS and nitrate concentrations in serum, apocynin reduced the cGMP and nitrite values while significantly elevating (p < 0.05) the eNOS concentrations and also improved the cadmium-induced anemia. Apocynin was effective in reducing cadmium-induced elevated blood pressures through elevation of eNOS. Inhibition of NADPH oxidase activity may be a useful strategy for prevention and treatment of cadmium-induced hypertension.
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