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The toxicity of 1-amino-3-chloro-2-propanol is associated with acute histopathological change in the medulla oblongata, characterised lesions of focal oedema. Continued administration results in neurological scars. Lesions can be induced at dose levels of 50 mg . kg-1 day-1. Clinical manifestations of neurological involvement are periods of slight incoordination and loss of balance in a few animals only.

The usefulness of measuring serum bile acid concentrations by RIA in a number of acute experimental liver injuries of rats was assessed by comparing the concentrations with the results of some of the routinely employed methods of examining hepatotoxic changes. Centrilobular liver cell injury produced by CCl4 revealed leakage of GPT and GDH and to a lesser extent AP; along with minimal increase in serum bile acid levels. Serum bilirubin concentration remained unchanged. Surgical bile duct ligation resulted in marked rises in AP, GPT and GDH and total bilirubin levels and levels of serum bile acids. Intravenous injection of MnSO4 induced focal necrosis of liver and bile canalivular dilation associated with elevated GDH and GPT concentrations. AP and bilirubin levels were unchanged. Bile acid levels were raised among female rats. 2,4-Xylidine induced hepatotoxicity revealed bile duct hyperplasia, liver cell enlargement, liver cell necrosis, biliary canalicular dilation and proliferation of endoplasmic reticulum. GDH and GPT levels were raised along with bile acid concentrations. This study suggested that assay of bile acid concentration is a sensitive indicator of several acute hepatic injuries.

One hundred and eighty Wistar-strain rats were exposed to differing concentrations of tobacco smoke, for periods of up to 20 months, in order to examine the response of the pulmonary immune system. The amount of bronchus-associated lymphoid tissue (BALT) in the lungs of exposed rats increased initially over the first 5 weeks of exposure, subsequently falling to below control levels by the fourteenth week and eventually increasing again to a level slightly higher than that of the controls by the twelfth month, at which level it was maintained until the twentieth month. Quantitative immunohistochemical assay of bronchial immunoglobulin levels (only assessed over the initial 14 weeks of exposure) revealed a transitory enhancement of levels followed by a depression, the speed of response being apparently dose-related. Alveolar macrophage activity, indicated by lysosomal enzyme activity, increased relative to the control animals over the same 14-week exposure period. The significance of these observations is discussed and a tentative explanatory hypothesis is advanced.

A number of instances have been reported in the scientific literature in which acute intoxication with halogenated oxyquinolines has led in some species to convlusions, often followed by death. The toxicity of repeated doses of clioquinol has been investigated extensively in the dog. The clinical syndrome induced in this species is characterized by anorexia, weight loss, extremem muscle weakness and emaciation. In some animals surviving this impairment of condition for several weeks, neuropathy of the central nervous system, but not of the peripheral nerves ensued. It is suggested that these toxicological manifestations are less dependent on the dose-level than on the degree of absorption. Some suggestions regarding the aetiology of the lesions are made.