Since the end of the nineteenth century, numerous cases of triorthocresyl phosphate (TOCP) poisoning due to accidental contamination of drink, food or drugs have been reported. Following the ingestion of preparations contaminated by TOCP, gastrointestinal symptoms may occur and after an interval of ten to twenty days, a well-known delayed neurotoxicity gradually develops. In general, the initial symptoms are pain and paresthesia in the lower extremities. In most cases, muscle weakness progresses rapidly developing into a striking paralysis of the lower extremities with or without an involvement of the upper extremities. Severe cases show pyramidal signs. The histopathological findings show axonal degeneration in the peripheral nerves and degenerative changes in the anterior horn cells. Degenerative change also occurs in the lateral and dorsal tracts of the spinal cord. The cardinal therapy is physical rehabilitation.
Materials and methods Male Wistar rats about seven weeks of age were randomly divided into four groups, and were acclimatised to the animal facility for one week before the start of exposure. The exposure system was the same as that described in our previous report.5 The food intake of control and lower dose groups was restricted according to the intake of the highest dose group to minimise differences due to nutrition. The rats in the exposed groups inhaled 50, 100, or 250 ppm of EO for six hours a day five days a week from Monday to Friday for 13 weeks. The rats in the control group were exposed to clean air in an identical system. Six rats were used in each exposed group and 12 in the control group. The concentrations of EO were repeatedly monitored by a gas chromatograph equipped with a flame ionisation detector.The rats were killed using an overdose of ether about 40 hours after the last exposure and the testes and epididymides were removed and weighed. One testis from each pair was fixed in Bouin's solution, embedded in paraffin, and stained with periodic acid Schiffreagent (PAS) and Gill's haematoxylin for light microscopical examination.5 The other testis was used for the measurement oflactate dehydrogenase X (LDH X) activity in the cytosol fraction. The decapsulated testis was homogenised in four volumes of 1-15% KC1 solution with a Potter-Elvehjem homogeniser. The homogenate was centrifuged at 105 000 g for 60 minutes, and LDH X activity was measured in the supematant by the method described by Meistrich et al 7 using a-ketovalerate, a specific substrate for this isozyme. Protein content of the cytosol fraction was determined by the procedure of Lowry et al.' One epididymis from each pair was divided into two portions (head and tail plus body) and sperm numbers in these portions were counted by the method described in our previous report.9 The appropriate part of the epididymis was homogenised in a 90 ml saline triton merthiolate solution (STM solution; 0-15 M NaCl, 0 05% (v/v) triton X-100, and merthiolate to give 0-25 M thimerosal) with a semimicro Waring blender for 1-5 minutes. Sperm present in the homogenates were counted with a haemocytometer. The tail of the other epididymis was opened by a razor and the sperm were squeezed into a 0-1 M sodium phosphate buffer, pH 7-2. The 270
A fatal case of acute fulminant hepatitis following exposure to dichloropropanols is reported. A 59-year-old male worker in a chemical plant developed general malaise, nausea and vomiting several hours after cleaning a tank that had contained dichloropropanols. He had no previous history of hepatic dysfunction. On admission, hepatomegaly was prominent. Because of highly elevated levels of GOT and GPT in the serum, reduced prothrombin time and a lowered consciousness level, a diagnosis of fulminant hepatitis was made. Significant decreases of leukocytes and platelets were also observed. Serum creatinine and BUN were slightly elevated. Although plasma exchanges were conducted on the third and fourth day, the liver functions continued to deteriorate. The patient died on the fifth day. Because dichloropropanols could be detected in the blood specimens obtained at the time of admission, we considered that fulminant hepatitis in this case was attributed to dichloropropanols exposure. To our knowledge, this is the first case of fulminant hepatitis after dichloropropanols-exposure.
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