BIOFARMASI J NAT PROD BIOCHEM Volume 18, Number 1, February 2020 E-ISSN: 2580-2550 Pages: 5-12 DOI: 10.13057/biofar/f180102 Protective effects of Curcuma longa rhizomes ethyl acetate extract against alcohol induced oxidative stress and nephrotoxicity in female Wistar rats O.E. ETENG 1 , C.A. MOSES 1 , J. ENOBONG 1 , A.J. AKAMO 1 , D.I. AKINLOYE 1 , R.N. UGBAJA 1 , O.A. AKINLOYE 2 1 Department of Biochemistry, Federal University of Agriculture. Abeokuta, Ogun State, Nigeria. email: ofemeffiom@gmail.com 2 Department of Biochemistry, University of Calabar. Calabar, Nigeria Manuscript received: 26 January 2020. Revision accepted: 4 February 2020. Abstract. Eteng OE, Moses CA, Enobong J, Akamo AJ, Akinloye DI, Ugbaja RN, Akinloye OA. 2020. Protective effects of Curcuma longa rhizomes ethyl acetate extract against alcohol induced oxidative stress and nephrotoxicity in female Wistar rats. Biofarmasi J Nat Prod Biochem 21: 5-12. This study aimed to evaluate the protective effect of Curcuma longa Linn. (syn. Curcuma domestica Val.) rhizomes ethyl acetate extract (CLREAE) facing alcohol-induced oxidative stress and nephrotoxicity. Thirty female (30) Wistar rats were categorized randomly into six groups. Groups 1, 2, 3, 4, 5 and 6 were treated with normal saline; 20% ethanol; 100 mg of CLREAE + 20% ethanol; 200 mg of CLREAE + 20%; 350 mg of CLREAE + 20% ethanol and 350 mg of CLREAE respectively for 14 days. A significant (p<0.05) decrease in the SOD, CAT and GPx activities and GSH concentration of rat treated with only 20% ethanol were found when compared to the normal control group, whereas a significant (P<0.05) increase in the groups pretreated with different doses of the CLREAE were also found when compared to groups with only 20% ethanol treatment. Thus, comparing to the normal control group, treatment with the CLREAE fetched a significant (p<0.05) decrease in the renal biomarkers (creatinine and urea). Whilst, comparing to the groups with 20% methanol treatment, a significant (p<0.05) increase happened in the groups pretreated with different doses of the CLREAE. There was a significant (p<0.05) decrease on Kidney MDA level in rats pretreated with different doses of CLREAE compared with the normal control. It was shown in the results of the histology that there was a physiologic recovery in the kidney tissues as groups were treated with different doses of the CLREAE. Evidenced by reduced necrosis of tubular and glomerular epithelial, the signs of protection against toxicity were found on the rats. The study suggested that through in vivo free radical scavenging ability, the CLREAE has protective effects against alcohol-induced oxidative stress and nephrotoxicity in female Wistar rats. Keywords: Nephrotoxicity, Curcuma longa, oxidative stress, alcohol, ethyl acetate INTRODUCTION Nephrotoxicity is the toxicity in the kidneys, and it is caused by toxic chemicals or medications having poisonous effects on kidney function. Several studies have identified that risk factors for nephrotoxicity involve alcoholism, high blood pressure, diabetes mellitus, exposure to occupational nephrotoxins and chronic use of analgesics (Knott et al. 1996). Alcohol and its metabolites go through kidneys and are excreted into urine, and its content in the urine is higher than that of the blood and the liver. The kidney is often involved in the development, maintenance and counter regulation of complex electrolyte disturbances (Das et al. 2008). As a risk factor for kidney damage, the blood pressure is being raised by regular alcohol consumption. Abnormalities in kidney structure and function are reported to have an increased frequency in fetal alcohol syndrome as seen in children prenatally exposed to ethanol. The kidney is an organ that is efficiently designed to perform two main tasks in the body, namely the excretion of metabolic end products and the proper regulation of body fluid constituents (Guyton 1992). When the tasks are completed, the kidney forms and collects urine, which passes through the ureter into the bladder (Rhoades and Pffanzer 1992). Nephrotoxicity determines xenobiotic damaging effects on the kidneys. Alcohol consumption has been related to a aloft incidence of coronary heart disease (CHD) and chronic kidney disease (CKD) (Parekh et al. 2001). Alcohol toxicity is linked to metabolism through alcohol dehydrogenase (ADH) which alters ethanol into toxic acetaldehyde which is eventually oxidized to acetate through aldehyde dehydrogenase (ALDH). Acetaldehyde is a toxic by-product of ethanol metabolites that causes liver defect (Purohit et al. 2003). Acute alcohol poisoning or chronic alcoholism causes kidney disablement (Knott et al. 2015). Other studies also denounce similar conclusions which shows that the incidence of kidney disablement is comparable or even lower in heavy drinkers (more than 210 g/week of alcohol consumption) than those in moderate drinkers (70-210 g/week of alcohol consumption) (Koning et al. 2015). On the contrary, several other studies have found that large amounts of alcohol consumption can predict worse outcomes in patients with chronic kidney sickness (White et al. 2009). For example, White and colleagues (Latchoumycandane et al. 2015) informed that heavier drinkers (those who consumed more than 30 g of alcohol/week) had a higher risk of developing albuminuria, which is usually a symptom of kidney sickness. There is