Effects of Oral Cadmium Exposure on Renal Glomerular and Tubular Functions in the Rat

The effects of orally consumed cadmium on the functions of the kidney have been investigated in rats based on the reported level of the toxicant in Warri River. Relative to the corresponding controls there were significant (P < 0.05) increases in the amount of cadmium in the kidneys of rats in all the test groups. Biochemical analysis revealed significant (P < 0.05) changes in plasma creatinine after 2 months (control – 1.20 ± 0.20 × 10; test – 0.92 ± 0.26 × 10 μg/ml) and glucose after 1-month (control – 91.67 ± 3.39; test – 102.75 ± 5.99 mg/dL) exposure. Twenty-four hours urine volume were significantly decreased (P < 0.05) in rats exposed to cadmium for 1 and 2 months. Also in the Cd-exposed rats urine protein was significantly elevated in those exposed for 2 and 3 months but their urine glucose was demonstratively elevated only in those exposed for 2 months (control – 33.00 ± 7.80; test – 43.00 ± 9.80 mg/dL). Urine creatinine was not significantly altered in any of the test groups. Consistently there were significant (P < 0.05) decreases in total ATPase and Mg ATPase activities at the end of the 2 and 3 months exposure when compared to the controls @JASEM The kidneys and liver are among the major target organs of cadmium (Cd) accumulation and intoxication (WHO report, 1992). The presence of cadmium in all links of the food chain, poor excretability, propensity for bioaccumulation and persistence make it a source of considerable risk to human health (Cabrera et al., 1998) vis-à-vis the functional integrity of the two organs indicated above and others. Cd-induced injury to both organs has been attributed to its ability to enhance free radical formation in vivo (Gupta et al., 1991; Bagchi et al., 1996). Some characteristic biochemical features associated with Cd-induced kidney damage are urinary excretion of protein, N-acetyl – β – D – glucosaminidase, glucose and amino acids. Others are marked increase of plasma creatinine or blood urea nitrogen levels (Horiguchi et al., 1996) as well as altered plasma glucose level (Chapatwala et al., 1980). Consumption of contaminated water is the major way by which humans are exposed to Cd (WHO report, 1992) and the maximum allowable level in drinking-water is 0.005 mg/dL (WHO report, 1984). In many countries including Nigeria contamination of rivers and adjoining seas by Cd and other heavy metals occurs in a number of ways among which is the discharge of waste liquid matter from industrial sites. The average level of Cd in Warri River waters between 1986 and 1991 was 0.3mg/L (Egborge, 1994). This is 60 – fold above the maximum allowable level in drinking water. Naturally this is worrisome. Therefore this paper focuses on the toxicity of Cd in rats, which can be related to the Warri River level of the toxicant within the period in question. MATERIALS AND METHODS Animals: Thirty-six adult albino rats (Wistar strain), 180 – 190g, bred in the Animal Unit of the School of Pharmacy, University of Benin were used for this study. Chemicals and reagents: Bovine serum albumin, cadmium sulphate (3CdSO4.8H2O), chloroform and sodium hydroxide were purchased from May and Baker, Dagenham, England. Adenosine triphosphate (disodium salt) was purchased from Sigma Chemical Company, U.S.A. Glucose oxidase kit was obtained from QCA (Spain). Treatment of animals: The rats were divided into six experimental groups of six rats each and housed in standard rat cages. From these, three subgroups made up of two cages of rat each were produced. One set of rats in a subgroup served as the control while the other served as the test. The control groups were provided with distilled water as drinking-water while the test groups were provided with aqueous solution of CdSO4 containing the equivalent of 0.30mg Cd/L for one, two and three months respectively. All rats were allowed free access to chow (BFFM, Ewu, Nigeria). Animal sacrifice and tissue preparation: After the specified period of exposure rats in each subgroup were transferred to metabolic cages equipped with accessory for collecting urine. The 24 hours urine samples were collected after which each rat was anaesthetized with chloroform. While under anaesthesia blood samples were obtained via heart puncture and transferred to heparinized tubes standing on ice. The kidneys were excised. Plasma was obtained by centrifugation at 3000 rpm for 10 minutes. The kidneys were homogenized as described by Adam – Vizi and Seregi (1982). JASEM ISSN 1119-8362 All rights reserved J. Appl. Sci. Environ. Mgt. 2004 Vol. 8 (1) 29 32 Full-text Available Online at http:// www.bioline.org.br/ja *Corresponding author: E-mail: Abstracts available Online at http://www.ajol.infos available Online at http://www.ajol.info Biochemical assays: The activities of ATPases in the kidney homogenates were assayed as described by Adam – Vizi and Seregi (1982). Protein content of the homogenate and urine was measured by the Lowry method as described previously (Obi et al., 1998). Plasma and urine glucose estimation was based on the glucose oxidase assay procedure described in the QCA kit instruction leaflet. Plasma and urine creatinine levels were determined by the Jaffe reaction in which a coloured product is formed from creatinine and picric acid in alkaline solution. Cadmium analysis: Kidney cadmium content was estimated with atomic absorption spectrophotometer (Varian AA 1475) after wet digestion of the tissues. For the digestion, 20ml HNO3 – HCLO4 mixture (4:1) was introduced into a beaker containing 1g of a given kidney sample followed by heating at 100oC until the sample was completely dissolved. Each digest was thereafter diluted to 100ml with distilled deionized water. Statistical analysis: The data are presented as means ± SD. The mean values of the control and test groups were compared using Student’s t-test. The significant level was set at P < 0.05. RESULTS AND DISCUSSION In this study we provided water and a solution of CdSO4 (≡0.30mg Cd/L) ad libitum to rats for oral consumption for 1, 2 and 3 months. At the end of each period of exposure the state of various plasma and urine parameters normally used as indicators of the proper functioning of the kidney were assessed. Changes in rat kidney Cd load caused by this treatment are presented in table 1. Table 1. Cadmium concentration in Kidney and Cd-exposed rats (mean ± sd); n = 6