Amikacin is an important antibiotic, and its use is limited because of the induced nephrotoxicity. Thus, search for natural and synthetic agents that can moderate amikacin toxicity never stopped. The present study aims to investigate the possible ameliorative effects of virgin olive oil and olive leaf extract against the amikacin-induced nephrotoxicity in rat.Methods48 rats were distributed into 6 groups: 1-Animals of control (C) group were injected intraperitoneally (ip) with saline, 2-(AK); injected ip with amikacin {300 mg/kg/day for 12days}, 3-(OO) group: given olive oil {7 ml/kg/day for 16days}, 4-(OOAK) group: given olive oil as in OO and amikacin for 12days, 5-(OL) group: given olive leaf extract {50 mg/kg/day for 16days}, 6-(OLAK) group: given leaf extract as in OL and amikacin for 12days. Animals were fasted and sacrificed. Serum was used for biochemical analysis and kidneys for histopathology.ResultsSerum urea and creatinine were significantly (P < 0.001) elevated in AK, and significantly dropped in the OOAK and OLAK groups. Serum uric acid was reduced in AK by 45.29%. Kidneys from AK showed necrosis, whereas, those from OOAK and OLAK showed mild histology. The serum triglyceride was decreased by 17.8% in OL, by 37.02% in OOAK and by 31.48% in OLAK. The calculated amikacin effect showed a significant positive correlation with urea (r = 0.521, P = 0.0004), and a negative correlation with uric acid (r = ⿿ 0.58, P < 0.0001).ConclusionThe study confirmed nephrotoxicity of amikacin in rat which was ameliorated by virgin olive oil and by olive leaf extract. Amikacin did not cause dyslipidemia but reduced serum uric acid.

Background: Cisplatin is a widely used anticancer drug. Its use is known to induce nephrotoxicity and may be associated with disturbance of the electrolyte balance. Spironolactone, an antagonist of aldosterone, is frequently prescribed as a potassium sparing diuretic. Aims and Objective: The present study aims to investigate whether spironolactone can correct the cisplatin-induced electrolyte disturbance in the rabbit. Materials and Methods: Thirty two New Zealand rabbits were distributed into four groups. Animals of control (C); spironolactone (S); cisplatin (P); spironolactone and cisplatin (SP) groups were injected ip with saline; given spironolactone (20 mg/kg bw/day) orally for 5 days; injected ip with cisplatin (6.5 mg/kg bw); given both spironolactone and cisplatin, respectively. Serum, liver and kidney cortical homogenates were used for biochemical analysis. Results: Serum creatinine and urea levels of P were significantly (P<0.001) elevated and were severely raised in SP by 7-fold and 2.7-fold. The serum magnesium was increased in S and SP groups by 93.75% and 112%, respectively and was depressed in P by 18.75% compared to C. Serum potassium and calcium of P were significantly (P<0.001) depressed, whereas, serum calcium levels in the S and SP were significantly elevated. The liver magnesium and calcium of SP were elevated by 38.37% and 40.7%, respectively, whereas, kidney magnesium showed reduction in the S, P and SP by 36%, 24% and 19%, respectively and elevated in the SP group by 26.56% compared to S group. The kidney calcium was depressed in the S, P and SP by 30.89%, 40.0% and 28.2%, respectively compared to C.Conclusion: Cisplatin treatment depleted the serum and renal cortical magnesium. The serum calcium and potassium were reduced secondary to the magnesium depletion. The co-administration of spironolactone reversed the cisplatin-induced magnesium and calcium depletions in serum and renal tissue.