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Adult female Rana ridibunda were exposed to 200 ppm (mg/l) of cadmium (Cd as CdCl2) dissolved in water for 4, 10, and 30 days. The 96-h LC50 value for Cd was determined to 534 ppm. The concentration of Cd in the liver and kidneys and the effect of Cd on the concentrations of hepatic metallothionein (Mts) and glutathione (GSH), were estimated. Cd accumulated in the liver and kidneys in a time-dependent pattern, with the kidneys accumulating the heavy metal at higher rates after the tenth day of exposure. There was a strong positive correlation of Cd concentration between these two organs. The concentration of Mts and GSH increased with the increase of Cd concentration in the liver, following a time- and Cd-dependence pattern. The concentration of Mts and GSH was positively correlated with the concentration of Cd in the liver. Mts concentration was positively correlated with GSH concentration.

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There are no data at present on the impact of lead (Pb) on amphibian metabolism, although declines of amphibian populations due to man-made changes in the environment have been recorded in recent years. We studied the impact of Pb on the liver metabolism of the frog Rana ridibunda by measuring the hepatic levels of glycogen, lactate, total fat, protein and glucose. Liver is one of the primary target organs of Pb bioaccumulation. Frogs were exposed for 4, 10 and 30 days to 14 mg l(-1) of Pb (in the form of Pb(NO(3))(2) dissolved in water) and compared with matched controls. The level of glycogen in the liver increased until day 30. The increase of the metabolite was time-dependent because there was a positive correlation (r = 0.994, P = 0.006) between glycogen concentration and the days of Pb exposure. Lactate concentration declined continuously up to day 30. Liver fat content decreased from day 10 to day 30. Protein concentration declined continuously until day 30. Glucose concentration increased up to day 30. Glycogen concentration was correlated negatively with liver fat content (r = -0.474, P = 0.005), liver protein content (r = -0.562, P = 0.0004) and lactate concentration (r = -0.472, P = 0.005), whereas it was correlated positively with the Pb burden of the liver (r = 0.578, P = 0.0005). The frog appeared to face a metabolic stress over the 30 days of Pb exposure, without being able to control it. We concluded that the increase of liver glycogen concentration was due to gluconeogenesis via lactate and lipolysis. Further experimentation on key gluconeogenic and lipolytic enzymes over the 30 days of Pb exposure would elucidate the mechanisms that may lead to such phenomena.