Abstract;Methylmercury chloride (MMC)-induced alterations in circradian sleep rhythmicity of the rat were statistically evaluated by application of cosinor method to hourly values of slow-wave sleep (SWS) and paradoxical sleep (PS) obtained4 days before and Days 23-26 after oral administration of MMC (15 mg/kg/day for 2 cosecutive days). The cosinor analysis revealed that the most prominent changefollowing MMC administration was a delay by 5 h of the circadian PS acrophase.Weattempted to elucidate the altered circadian PS rhythm in the term of brain noradrenaline (NA) metabolism. Rats administered orally with MMC at the same dose orwith a vehicle solution as a control were sacrificed by decapitation at 6 different times on Day 23 after the first administration. Noradrenaline (NA) and 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG) of the frontal cortex and the hippocampus were determined by high-performance liquid chromatography with electrochemical detection. Cortical NA levels of the MMC-administered rats were significantly lowered at 0200 h and 0600 h, as compared to those of the control rats. Cortical MHPG level of the MMC-administered rats increased significantly at 1000 h and then decreased significantly at 2200 h, whereas hippocampal MHPG levels of the MMC-administered rats decreased significantly at 1800 h and 2200 h. A plausible mechanism underlying the MMC-induced delay in the circadian PS acrophase was discussed in the light of cortical and hippocampal changes in NA metabolism.
The effects of mono-, di-, and tributyltin, which are widely used in industry, on human platelet aggregation were studied in vitro. The results demonstrated that these organic butyltin compounds inhibit epinephrine-induced aggregation. The antiaggregating concentrations (IC50) of the butyltin compounds were 10 nM for tributyltin, 10 μM for dibutyltin and 500 μM for monobutyltin. However, none of these compounds affected the platelet aggregation induced by others stimuli (ADP, arachidonate, and collagen). On the other hand, all of the butyltin compounds inhibited the binding of |3H|-DHEC to human platelets, and di-and tributyltin significantly inhibited the incorporation of |14C|-epinephrine into gel-filtered platelets. These results indicate that organic butyltin compounds inhibitepinephrine-inducedaggregation by blocking the epinephrine bindingto human platelets.
Administration of nickel (50 μ moles Ni/kg as NiCl2•6H2O, subcutaneously) to partially hepatectomized rats at 8, 16, 24 and 72 hrs revealed that it did not produce any change in the levels of hepatic or renal glutathione at any time interval when compared with saline treated hepatectomized rats. Remarkable changes were however observed in glutathione-S-transferase and phosphoglucomutase at 16 and 24 hrs in liver while only at 8 hrs in kidney. The effect of various doses of nickel (50, 100 and 150 μ mole Ni/kg) at 16 hrs revealed that 100 μ moles nickel produced maximum enhancement in the levels of all these parameters in liver while in kidney practically no change was observed.
The level of urinary δ-aminolevulinic acid (ALA) has been widely used as a measure of the biological effect of lead. The determination of urinary ALA has been carried out using ion-exchange column chromatography which is necessary for removal of interfering substances present in the urine, namely, porphobilinogen, urobilinogen and urea.1-3) These methods are more accurate for determining ALA in urine, but are time-consuming in large-scale routine analysis. A simpler and more rapid method for the determination of urinary ALA using liquidliquid extraction instead of column chromatography was developed in 1972.4) Presently, this simple method is widely used for the routine screening of workers exposed to lead. In this procedure, ALA-pyrrole is separated from most of the interfering substances present in the urine by extraction with ethyl acetate. Recently, we found that the recovery of ALA from normal urine is inversely correlated with the urine density, when urinary ALA is determined by this simple