Comparative biochemistry and physiology. C, Comparative pharmacology and toxicology最新文献

The sympathomimetic amines tested, including those of alpha and beta type, were all ineffective in arousing melanosome aggregation within dermal and epidermal melanophores of the siluroid catfish, Parasilurus asotus. Conversely, these amines unfailingly gave rise to a dispersion of the pigment. While alpha-adrenergic blocking agents had only a little influence, beta agents exhibited a strong inhibitory effect on the pigment-dispersing action of the amines. Electrical nervous stimulation failed to bring about a melanosome dispersion. It was concluded that the adrenoceptors possessed by dermal and epidermal melanophores of this species seemed to be solely of the beta-adrenergic type, mediating the pigment dispersion, and that the endogenous amines involved in the darkening reaction of animals may originate in adrenal chromaffin cells, and thus are not derived from the peripheral nervous elements.

Mechanisms controlling pigment movements in the melanophore of the blue damselfish, Chrysiptera cyanea, were studied. Histological observations revealed that the melanophore had three-dimensionally developed processes to envelop overlying small iridophores, and thus participated in the construction of a simple dermal chromatophore unit. Nervous stimulation, catecholamines and melatonin brought about melanosome aggregation in the melanophore. The actions of the nervous stimulation and catecholamines were antagonized by alpha adrenolytic agents. A beta adrenergic agonist, metaproterenol, adenosine and adenine nucleotides, and alpha-MSH acted as pigment-dispersing agents. These results indicate that the melanophore of the present material is controlled quite orthodoxly by adrenergic nerves and endocrines, notwithstanding the fact that it has quite a unique morphology among fish species, and that its motile rate is remarkably high.

Pretreatment with acebutolol or propranolol at high concentrations had an inhibitory effect on the contractile response to 5-hydroxytryptamine (5-HT) in most vascular smooth muscles such as rabbit aorta and basilar, mesenteric, renal, femoral arteries and cat coronary artery. The inhibitory actions of both agents were generally greater than on the responses to excess Ca2+ and potassium. In rabbit renal arteries, acebutolol had no effect on the response to 5-HT but inhibited the responses to excess Ca2+ and potassium. Propranolol had a marked inhibitory effect on the response to 5-HT. In all preparations used, the contractions induced by norepinephrine (NE) and histamine showed a much greater resistance to the effect of acebutolol and propranolol than the contractions induced by 5-HT, Ca2+ and potassium. Nifedipine had no inhibitory effect on the response to 5-HT in most of the preparations. Nifedipine inhibited the response to 5-HT only in the basilar arteries. The inhibitory actions of propranolol on the response to 5-HT was greater than that of acebutolol. The inhibitory action of acebutolol and propranolol on the response to 5-HT may be related to mechanisms other than the beta-adrenoceptor blocking action of the drugs. The possible mechanisms of inhibitory action of both beta-adrenoceptor antagonists on 5-HT are discussed.

The content of cytochrome P-450 and the specific activity of laurate hydroxylation have been measured at monthly intervals through the year in liver microsomes of males and females of Japanese bullfrog, Rana catesbeiana. The specific activity, based on microsomal protein or cytochrome P-450 of both sexes was higher in spring (April-May) than in autumn (October-November) and the difference was statistically significant. However, in males the content of the cytochrome P-450 in the spring was almost the same level as in the autumn and it was rather lower in the spring than in the autumn in females. These suggest that the cytochrome P-450 species catalyzing laurate hydroxylation increased specifically in the spring. The specific activity (based on cytochrome P-450) in males was significantly higher than that in females in spring (April-May) or autumn (October-November).

In vitro addition of cadmium chloride (CdCl2) to a reaction mixture decreased the liver microsomal cytochrome P-450 level of the male guinea-pig. In contrast nickel chloride (NiCl2) did not cause any alteration in the cytochrome P-450 level. Neither CdCl2 nor NiCl2 produced any activity changes in the liver microsomal NADPH-cytochrome c reductase. When the liver microsomes were preincubated in the presence of CdCl2, metal-induced reduction increased as the time of preincubation progressed and attained its maximum reduction level at about 15 min. In the case of NiCl2, the maximal reduction level was attained at about 5 min. However, no changes were observed by metals in liver microsomal NADPH-cytochrome c reductase activity as the time of preincubation progressed. After preincubation, the reduction of cytochrome P-450 achieved by CdCl2 was stronger than that obtained by NiCl2 as well as than that obtained by CdCl2 without preincubation.

The stimulatory effects of calcium alpha-glycerophosphate (CaG) and Ca2+ on the generation of medullary prostaglandin E2 have been compared. CaG (4mM) was significantly more effective than Ca2+ (4 mM) as a stimulus for prostaglandin E2 release. This effect of CaG was most pronounced in the presence of exogenous phospholipase A2 (0.1 unit/ml). These results suggest that CaG has a more powerful stimulatory effect on prostaglandin E2 formation than Ca2+ because of its high affinity for phospholipase A2.

The effects of DDT and dieldrin on cholinergic neurotransmission were studied using the sixth abdominal ganglion of the cockroach. Spontaneous electrical discharges in the ganglion recorded with an extracellular electrode were augmented by 0.1 mM DDT and 1 microM dieldrin. This stimulating action was partly blocked by 0.5 mM d-tubocurarine and 0.1 mM hemicholinium-3 and disappeared in a high Mg2+-low Ca2+ medium. DDT and dieldrin increased both ACh release and ACh content in the ganglion. These results suggested that DDT and dieldrin stimulate both ACh release and synthesis.

A relatively high concentration of metallothionein was present in the liver of the control mature tortoise Clemmys mutica. The administrations of cadmium and copper to Clemmys mutica increased the metals in the liver with concomitant decrease of zinc, which was due to substitution of zinc in the native metallothionein with cadmium and copper. The Clemmys metallothionein was a mixture of three isoproteins which were abundant in half-cystine (34.2-34.6 mol%) and lysine (10.8-11.9 mol%), but lacked aromatic amino acids. One of the isoproteins, MT-I, contained one residue of histidine, which was an identical feature with frog and avian metallothioneins.

Plasma levels of lactate and oxypurines markedly increased in both fed and fasted rats exposed to three acute anoxic states, cyanide poisoning, carbon monoxide poisoning and inhalation of oxygen-deficient gas, suggesting that the transition of aerobic to anaerobic metabolism occurred similarly in both groups. Plasma glucose level of fed rats increased 1.8-2.5 times after exposure to anoxia, whereas a remarkable hypoglycemia was induced by the exposure of fasted rats to anoxia. Hepatic glycogen stores in fed rats induced hyperglycemia, while exhaustion of the stores in fasted rats resulted in severe hypoglycemia during acute anoxia.