Neurotoxic effects of the combined exposure to carbon disulphide and ethanol in rats.

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.

Dissociation between circling behaviour and striatal dopamine activity following unilateral deltamethrin administration to rats.

The neurotoxic pyrethroid, deltamethrin, induces a severe motor syndrome characterised by tremor and choreoathetosis when injected systemically to rats. The interaction between deltamethrin and the two major dopaminergic pathways - the nigrostriatal and mesolimbic pathways - was investigated in rats. Striatal catecholamines, indoleamines and metabolites were measured by HPLC with electrochemical detection.

Nephrotoxic effect of trimethyltin in rats.

Male Wistar (Porton) rats were dosed by gavage with trimethyltin chloride in arachis oil at doses of 3, 6 and 10 mg/kg. Water consumption and urine production were monitored for 3 days after dosing and at the end of this period the rats were killed and the kidneys were examined histologically. Within 6 h of dosing there was an increase in urine production and in the pH of the urine in all treated groups.

Effect of alcohol intake on some disturbances induced by chronic exposure to carbon disulphide in rats. II. Biochemical and ultrastructural alterations in the peripheral nerves.

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.

Effect of alcohol intake on some disturbances induced by chronic exposure to carbon disulphide in rats. I. Behavioural alterations.

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.

Effect of cadmium on arterial blood pressure and lipid metabolism in rats.

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.

Effect of inhalation exposure to cadmium oxide on arterial blood pressure, lipid metabolism and tissue cadmium concentration in rats.

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.

[Diurnal rhythm of the bioelectrical activity of the brain and blood serotonin level in patients with migraine].

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.

Effect of different conditions of acute exposure to carbon monoxide on the cerebral high-energy phosphates and ultrastructure of brain mitochondria in rats.

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.

Biochemical alterations in the peripheral nerves of rats intoxicated with carbon disulphide.

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.

The content of high-energy phosphates and ultrastructure of mitochondria in the brain of rats exposed to carbon disulphide.

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.