Biomedical subjects
R von Burg
Publications and source records attributed to R von Burg.
Oxygen consumption of rat tissue slices exposed to methylmercury in vitro.
The physiological significance of damage from methylmercury exposure was assessed by comparing the oxygen consumption of rat liver, kidney and brain tissue slices after direct exposure to methylmercury chloride. Standard Warburg respirometers were used. Methylmercury chloride was added during the preparation of the experimental flasks and the tissues were preincubated for up to one hour. Oxygen consumption was accelerated by tipping sodium succinate into the main chamber from the sidearm. During the ensuing 3 h of observation, oxygen was consumed at a uniform rate and all the organ slices were equally inhibited at the respective concentrations of methyl-mercury tested. Brain slices without excess succinate were slightly more sensitive to the presence of methylmercury, but this difference was significant only at 2 . 10(-4) M methylmercury. The results suggest (a) that all three organs are about equally sensitive to direct toxic insult by methylmercury under standardized conditions, (b) that any difference observed is due to metabolic reserve capacity and (c) that organ damage induced by methylmercury cannot be attributed to a direct interference with the glycolytic machinery of the cells since organ tissue levels at the point of intoxication are considerably lower.
Methylmercury and the skeletal muscle receptor.
Methylmercury at bath concentration of 2 X 10(-5) M was capable of inhibiting muscular contractions of the isolated rat phrenic-nerve hemidiaphragm preparation. At the height of inhibition, nerve action potential could still be recorded and the muscles continued to respond to direct stimulation. The inhibition was not reversible with L-cysteine or D-penicillamine but limited protection was possible by prior treatment with (+)-tubocurarine. Treatment of frog rectus muscles with methylmercury (0-2 mM for 15 min) resulted in a shift to the right of 1 log unit in the dose response curve to acetylcholine and a reduction in the maximum response of the tissue. The observed inhibitory action of methylmercury on neuromuscular transmission may be explained by an action on the disulphide bond believed to be present on a cholinergic receptor.