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Investigations of biological rhythms were done in migraine relating the results to certain neurochemical and electroencephalographic studies. The obtained results demonstrated evident individual fluctuations of blood serotonin level in patients with migraine and in control groups. Correlations and connections were demonstrated between the blood serotonin level and EEG pattern and type of migraine. This suggests that the pathomechanism of migrainous headaches may be not homogenous.

Some biochemical correlates of Wallerian degeneration of the peripheral nerve were compared in carbon disulphide (CS2) and acrylamide-induced neuropathies. Rats were exposed to CS2 at two concentrations (1.5 mg/l and 0.8 mg/l air). An increase in the activities of beta-glucuronidase and acid phosphatase, in the ratio of cholesterol esters to free cholesterol (E/F) and a decrease in phospholipids in the sciatic nerve of rats exposed to CS2 was found. The magnitude of these changes was related to the concentration of CS2 and the alterations were similar to those observed in the sciatic nerve of rats intoxicated with acrylamide.

The arterial blood pressure, lipid content in serum and some organs, cadmium level in blood, aorta wall, lung and liver have been examined in rats repeatedly exposed to cadmium oxide fume 5 hours daily, 5 days a week, during 6 months. The blood pressure in rats exposed to cadmium oxide at concentration 0.02 mg Cd/m3 and 0.16 mg Cd/m3 was not changed, but it was slightly lowered at concentration 1.0 mg Cd/m3, which has been found lethal for rats. The concentration of total cholesterol, phospholipids and cholesterol esters in serum of female rats exposed at concentration of 0.16 mg Cd/m3 for 3 months was decreased, but was not affected after 6 months of exposure. The content of cholesterol and triglycerides in aorta wall, heart and liver was unchanged, although the content of cholesterol was decreased in adrenals of rats exposed for 3 months at concentration of 0.16 mg Cd/m3. Inhalation of cadmium oxide brought about the marked increase of Cd content in lung and kidney of rats exposed at all concentrations an increase of Cd blood level in rats exposed at concentrations of 0.16 mg Cd/m3 and 1.0 mg Cd/m3 and no increase of Cd content in aorta wall.

The effect of chronic ethanol (EtOH) administration on CS2-induced peripheral neuropathy in rats was studied. Rats were exposed to 0.8 mg/l CS2 for 12-15 months and to 10% EtOH as only drink during the last 4 months of the experiment. Some biochemical correlates of Wallerian degeneration of the peripheral nerve were estimated and ultrastructural examinations of the peripheral nerves were performed. It was shown that EtOH augmented the alterations in lipid content provoked by CS2 in the peripheral nerves, i.e. an increase in cholesterol esters and in the ratio of cholesterol esters to free cholesterol (E/F ratio) and a decrease in phospholipid content. The magnitude of ultrastructural changes induced by CS2 in the nerves was increased by EtOH.

Neurotoxic effects of the combined exposure of rats to carbon disulphide (CS2) and ethanol (EtOH) were studied. Biochemical and ultrastructural evaluation of the central nervous system (CNS) and peripheral nervous system (PNS) was performed. Male Wistar rats were exposed to CS2 vapour (0.8 mg/l air) and to 10% alcohol in the drinking water for 8 months. EtOH elevated the increase in beta-glucuronidase activity caused by CS2 in the hippocampus and in the cerebral cortex. No effect on the high-affinity synaptosomal uptake of L-glutamate and GABA was observed and no marked ultrastructural changes in the tested brain regions were found. In the peripheral nerves CS2 alone evoked axonal degeneration whereas CS2 combined with EtOH caused disturbances in myelin. Ultrastructural changes preceded biochemical alterations in the PNS and the biochemical indicators of peripheral neuropathy such as beta-glucuronidase activity and cholesterol ester content were not significantly affected. It is suggested that CS2 and EtOH combined affect both PNS and CNS to a higher extent than each of these substances alone.

Rats were exposed to carbon monoxide (CO) in different conditions: 4 min at 1.3% CO, 40 min at 0.5% CO or 12 h at 0.13--0.15% CO. After 4 min exposure to 1.3% CO the brain content of ATP and PC was substantially reduced; after 40 min exposure to 0.5% CO the cerebral ATP level was slightly increased, whereas the content of both ATP and PC in the brain of rats exposed to CO for 12 h was significantly higher than in the controls. The decrease in the brain level of ATP and PC after 4 min exposure to 1.3% CO was accompanied by ultrastructural changes of mitochondria. No evident differences in the level of cerebral high-energy phosphates were found between rats intoxicated with CO and rats subjected to experimental hypoxemia.

A total dose of 8 mg cadmium acetate/kg body weight was administered by repeated i.p. injection to female Wistar rats for 12 weeks. Slight, but significant, increases in blood pressure were recorded. The lipid concentration in serum and other tissues examined was not significantly affected, apart from a decrease in hepatic triglyceride. The blood cadmium (Cd) concentration was increased 10 times and Cd in the aortic wall was 4 times higher in treated rats. Cd affects hepatic lipid metabolism and it is considered that the increase in blood pressure is associated with accumulation of Cd in the arterial walls.

Rats were exposed to carbon disulphide (CS2) continuously for 12 h or for 10 months, at concentrations of 2.4 mg/l air and 0.8 mg/l air, respectively. No changes in the brain content of ATP, ADP and AMP were found in rats after chronic exposure, whereas the content of ATP in the brain of rats acutely poisoned with CS2 was significantly higher (21%) accompanied by decrease in the content of ADP (10%) and AMP (45%). The biochemical changes were accompanied by ultrastructural changes of mitochondria, particularly those in the cerebellar perikaryons.

Female white Wistar rats were exposed to CS2 vapour (0.8 mg CS2/1 air) 11 months and to 10% ethanol as the only drinking liquid for the last 3 months of exposure. Spontaneous exploratory motor activity (SEMA), open-field behaviour, passive avoidance performance and the avoidance acquisition were tested. Ethanol did not change the exploratory motor activity and behaviour of CS2-exposed rats in the open-field and passive avoidance tests but it affected their performance in the conditioned avoidance test. The analysis of data suggests that ethanol may adversely affect memory and learning ability in CS2-exposed rats.