Hepatorenal protection of food supplement (Prosopis africana) in rat following metal mixture exposure via alternations in oxido-inflammatory markers

Abstract

Chronic exposure to heavy metals can cause extensive damage to multiple organs and increase the risk of chronic diseases. This study has evaluated the effects of Prosopis africana (PA) on heavy metal mixtures (HMM) induced hepato-renal toxicity in Sprague Dawley rat. Twenty-five male albino Sprague Dawley rats were randomly assigned to five groups subjected to different treatments. Control (group 1) received deionized while the positive group (group 2) received HMMs: PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), HgCl2 (0.40 mg/kg), and NaAsO3 (10 mg/kg). Groups 3, 4, and 5 were also exposed to the HMMs plus PA at doses of 500, 1000, and 1500 mg/kg, respectively. All treatments were through oral gavages for 60 days. The rats were sacrificed under pentobarbital anesthesia, and blood, liver and kidney were collected for biochemical and histopathological studies. HMM exposure showed significant (p < 0.05) decrease in feed and fluid intake, initial, final and percentage body weight. The absolute and relative liver and kidney weights increased and higher levels of Pb, Cd and As were detected in HMM only group than in the other groups. There were significantly (p < 0.05) raised levels of Malondialdehyde (MDA) and nitric oxide (NO) (0.79 ± 0.01 uM/ml/mg and 86.01 ± 0.01 µM), tumor necrosis factor-α (TNF-α) (1217 ± 3.53(pg/ml), interleukin-6 (IL-6) (770 ± 1.41 pg/ml), Caspase- 3(22.25 ± 0.63 ng/ml), Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) (274 ± 2.83 (pg/ml) and nuclear factor-κB (NF-kb) (2.75 ± 0.02 ng/ml) with significant (p < 0.05) reduction in superoxide dismutase, glutathione peroxidase, catalase and reduced glutathione (1.67 ± 0.01 µg/ml/mg, 0.29 ± 0.01 µg/ml/mg, 0.11 ± 0.0 µg/ml/mg and 1.68 ± 0.01 µg/ml/mg) in comparison to the deionized water treated group. Taken together, the results showed that PA may be protective against metal induced hepatorenal damage via alternations in Nrf2-NF-kb pathway.