No abstract

This study describes a long-term test over three generations, using zebrafish (Brachydanio rerio) as the test species and concentrations of 1, 0.2, and 0.04 mg/L 4-chloroaniline (CA) as a model substance. The effect of the compound on the ecologically important parameters reproduction and growth was the focus of interest. Reduction in egg release by fish raised under CA was the most sensitive parameter in the test. Compared to the toxic threshold concentration for growth (0.4 mg/L), egg release was affected by a ten-fold lower concentration (0.04 mg/L). This study demonstrates that a long-term test is still the most appropriate method to assess the chronic toxicity of a substance on fish. A chronic toxicity test is proposed which comprises two generations, with the zebrafish as test species.

The effects of acetylcholine on glucose and lactate balance and on perfusion flow were studied in isolated rat livers perfused simultaneously via the hepatic artery (100 mmHg, 25-35% of flow) and the portal vein (10 mmHg, 75-65% of flow) with a Krebs-Henseleit bicarbonate buffer containing 5 mM-glucose, 2 mM-lactate and 0.2 mM-pyruvate. Arterial acetylcholine (10 microM sinusoidal concentration) caused an increase in glucose and lactate output and a slight decrease in arterial and portal flow. These effects were accompanied by an output of noradrenaline and adrenaline into the hepatic vein. Portal acetylcholine elicited only minor increases in glucose and lactate output, a slight decrease in portal flow and a small increase in arterial flow, and no noradrenaline and adrenaline release. The metabolic and haemodynamic effects of arterial acetylcholine and the output of noradrenaline and adrenaline were strongly inhibited by the muscarinic antagonist atropine (10 microM). The acetylcholine-dependent alterations of metabolism and the output of noradrenaline were not influenced by the alpha 1-blocker prazosin (5 microM), whereas the output of adrenaline was increased. The acetylcholine-dependent metabolic alterations were not inhibited by the beta 2-antagonist butoxamine (10 microM), although the overflow of noradrenaline was nearly completely blocked and the output of adrenaline was slightly decreased. These results allow the conclusion that arterial, but not portal, acetylcholine caused sympathomimetic metabolic effects, without noradrenaline or adrenaline being involved in signal transduction.

In perfused rat liver perivascular nerve Stimulation (7.5 Hz, 20V, 2 ms, 5 min) at the liver hilus caused an increase in glucose release, a shift of lactate uptake to output and a decrease in arterial, portal and total flow. The influence of the a r receptor blocker prazosin and the ß-antagonist propranolol on these nerve effects were studied in the isolated rat liver perfused via both the hepatic artery and the portal vein in three experimental series at 9 a.m., at 2 p.m. and at 8p.m.1) The nerve stimulation-dependent increase in glucose output was maximal at 9 a.m. (100%), halfmaximal at 2 p.m. (50%) and very low at 8 p.m. (15%). The alterations in arterial, portal and total flow were similar in all three series.2) At 9 a.m., at 2 p.m. and at 8 p.m. 5 arterial plus portal prazosin nearly completely inhibited the metabolic alterations and blocked the reduction of arterial, portal and total flow by 80%. 3) At 9 a.m., arterial, portal and arterial plus portal propranolol inhibited the increase in glucose release to less than 25% and the shift of lactate uptake to output to about 50%. At 2 p.m. this inhibitory effect was not observed, neither by selective arterial or portal, nor by simultaneous arterial plus portal addition of propranolol. At 8 p.m. the influence of propranolol could not be studied because of the too small control values. The nerve stimulation-dependent reduction of arterial, portal and total flow was not influenced by propranolol, neither at 9 a.m. nor at 2p.m. The results allow the assumption, that /3-receptors showed a circadian variation being involved in metabolic nerve actions only during the early phases of the light period.