There are few data at present on the impact of lead (Pb) on amphibians, although declines in amphibian populations due to man-made changes in the environment have been recorded in recent years. The impact of Pb in adult frogs, Rana ridibunda, was therefore examined. Animals were exposed to 14 mg l(-
Exposure of Rana ridibunda to lead II. Impact of lead on various parameters of liver metabolism of the frog Rana ridibunda
✍ Scribed by Angelos K. Vogiatzis; Nikolaos S. Loumbourdis
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 93 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0260-437X
- DOI
- 10.1002/jat.753
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✦ Synopsis
Abstract
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. Copyright © 2001 John Wiley & Sons, Ltd.
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