[Activity of choline esterases in blood cells and serum and cobalt activated acylase in toxic and non-toxic liver damage].

Organic insecticides used in agriculture and drugs often taken without medical control remain an important source of intoxication. The significance of the problem has been discussed in American medical literature, where toxic and posttoxic damage to the liver is rated second (25%), just after viral damage (40%), like in other highly developed countries. It can be assumed that the leading position of viral damage is the result of difficulties in ascertaining the diagnosis in each case of the disease. Clinical diagnosis of liver damage, in spite of many laboratory methods described and in use, leaves a margin of uncertainty and error. The diagnosis relies heavily on the activity of enzymes characteristic for morphologic and functional status of the liver. The determination of enzyme activities in plasma is also one of the basic diagnostic tools in the toxicology clinic in all cases of intoxication by hepatotoxic compounds. Toxicological recognition of acute intoxications relies on a wide range of biochemical tests and enzyme indices to evaluate the extent of damage by xenobiotics to organs. Usually the tests are selected in a clinical setting when the cause of intoxication is known. The present data were supplemented with activities of AspAT and AlAT determined during hospitalization of the patients. This choice acknowledged the wide-spread use of these tests and their organ specificity. All parameters in the control group were within normal limits described in the literature. For patients with phosphoroorganic or carbaminate intoxications (Ia) the activity of AECh and ECh proved to be a specific and sensitive parameter. In these cases both activities showed large, significant drops, confirming earlier reports advocating the use of these tests in insecticide intoxications. (Tab. 1-3). Among clinical symptoms frequently accompanying intoxication by ethylene glycol (Ib) one would mention metabolic acidosis, kidney damage and narcotic action of the glycol on the CNS. Little attention has been devoted to the hepatotoxic action of this compound. In the present study activities of the aminotransferases deviated slightly from normal. The DeRitis index was also within normal limits. However, the activity of AACo in this group of patients differed significantly from the control values. In the group of patients with Amanita phalloides poisoning (Id) the most sensitive indicator of liver damage proved to be AACo. The activity of this enzyme was significantly higher than in the remaining groups. The rise of activity of this enzyme was significantly higher than in the remaining groups. The rise of activity preceded by a few hours the appearance of increased aminotransferase activity which was observed near the end of the second day after intoxication. In the group of patients with chronic active hepatitis (II) the only parameter within normal limits was ECh. This finding supports earlier reports as to the relatively late decrease in the rate of synthesis of this enzyme in liver diseases. The use of toxogonine in vitro to discriminate between ECh and AECh in intoxications and liver diseases was decided upon basing on numerous reviews describing the clinical applications of this agent. The results of agent in the toxogonine test are in line with the disruptive action to toxogonine on the enzyme-insecticide complex in vitro, probably similar to the situation in the living organism. The observed elevation in AECh activity after the enzyme was inhibited by the phosphoro-organic pesticide, observed 30 minutes since the addition of toxogonin, averaged 86% +/- 25%. In the case of carbaminate insecticides the addition of toxogonine was followed by a further decrease in esterase activity and only a few samples showed an increase, but not exceeding 25%. No effect of toxogonine was seen in the case of serum cholinesterase and after 30 minutes the activity continued to fall.