Comparative biochemistry and physiology. C: Comparative pharmacology最新文献

1. The properties of the oocyte membrane adenylate cyclase system of the starfish Aphelasterias japonica at different stages of gametogenesis were studied.

2. The adenylate cyclase activity of fully grown oocytes was insensitive to catecholamines whereas activity in growing oocytes was increased.

3. Forskolin and NaF stimulated catalytic activity of growth and fully grown oocytes to various degrees. The stimulated effect of these modifiers was more considerable in grown oocytes.

4. We believe that the interaction between components of the adenylate cyclase system is altered in gametogenesis.

1. Proline was found to be the major component of CTC-12 (44%) and FSS II (45%) strain.

2. The cypermethrin treatment resulted in an increase in most of the amino acids of sixth instar larvae and all amino acids of adult beetles of CTC 12 strain.

3. In the susceptible strain (FSS II), however, the tyrosine, phenylalanine and arginine increased, whereas serine, proline, glycine, alanine, valine, isoleucine, leucine and lysine were decreased significantly in the sixth instar larvae.

4. In the FSS II adult beetles, only aspartic acid increased, while other amino acids either decreased (threonine, proline, glycine, alanine, valine, methionine, isoleucine, tyrososine, lysine, arginine) or remained unaffected (serine, glutamic acid, leucine, phenylalanine, histidine).

1. The roles of the inhibitory neurotransmitter GABA and the excitatory neurotransmitter glutamate in anoxic survival and anoxic death are discussed, with particular reference to the brain.

2. It is pointed out that the metabolic relationship between GABA and glutamate causes the neural levels of GABA to increase and glutamate to decrease during anoxia.

3. It is suggested that increased levels of GABA could mediate metabolic depression, and, thus, anoxic survival in ectothennic as well as endothermic vertebrates. Furthermore, evidence for a role of GABA in hibernation is discussed.

4. A hypothesis is presented suggesting that hypoxia has been a selective pressure in conserving GABA and glutamate as major inhibitory and excitatory neurotransmitters in vertebrates as well as invertebrates.

1. The 96-hr lc₅₀ values for juvenile hard clams, Meretrix lusoria, were 328, 392 and 194 μg/l Hg in 10, 20 and 30 ppt salinities at 25 ± 1°C, respectively; for adult hard clams 341 and 140 μg/l Hg in 20 and 30 ppt salinities, respectively.

2. Acclimatizing the adult clams to low salinity of 10 ppt lessened the toxicity of mercury. However, juvenile animals appeared to be more sensitive to mercury poisoning after 96 hr exposure in 10 ppt salinity.

3. All embryos exposed to 40 μg/l Hg and above died within 30 hr. In the control, 44% of hatched embryos had developed into D-stage larvae, while those exposed to 20 μg/l Hg were still in the trochophore stage. Most of the retarded larvae developed into abnormal forms within 30 hr at 28°C in 15 ppt salinity.

4. In order to maintain water quality and protect natural resources, the recommended safe level of mercury is 0.046 (0.039–0.053) μg/l Hg, based on the estimated 30-hr EC₅₀ for the clam embryos, with an application factor of 0.01.

1. Langendorff-perfusion of rat hearts with either 10 mM caffeine or 1 mM 2,4-dinitrophenol (DNP) caused severe ultrastructural damage to the myofilaments and mitochondria that was similar to that found in a standard Ca²⁺-paradox.

2. This damage occurred in the presence and absence of extracellular Ca²⁺

3. Creatine kinase (CK) release (indicative of sarcolemma breakdown) was not recorded unless the caffeine- or DNP-perfusion was preceded by Ca²⁺₀-depletion.

4. It is concluded that: (i) the pathways leading to damage to the myofilaments and sarcolemma are independent; (ii) the CK release mechanism requires dual activation of Ca²⁺₀-depletion plus a rise in [Ca²⁺]_i; and (iii) current theories concerning the mechanisms underlying the genesis of the Ca²⁺-paradox are incorrect or incomplete.

1. Changes in the erythrocyte system of frogs poisoned with tetrachlorwinfos depend on the sex of the animals and the dose of pesticide applied. They are a result of the pathomorphological changes due to translocation of fluids from the tissues to the circulation and swelling of the blood cells.

2. Changes in the leucocyte system of frogs are caused by several mechanisms: lytic action of the pesticide on the blood cell membrane, the stressogenic effect of the agent and enhanced activity of the reticuloendothelial system.

3. The appearance of typical changes due to stress, after even the lowest dose of tetrachlorwinfos, and low ld₅₀ values indicate that this pesticide is highly toxic for frogs.

4. The relatively high susceptibility of frogs to intoxication with tetrachlorwinfos is probably the result of a high affinity of cholinesterase to this pesticide, because of the presence of the P=O bond in its molecule.

1. The pharmacological properties of four synthetic analogues of the wasp neurotoxin, Vespulakinin 1, were studied using a cascade of mammalian smooth muscle preparations and the synaptic transmission from the cockroach cereal nerves to a giant interneuron.

2. All analogues have an extremely slow bradykinin-like effect on the smooth muscles. The carbohydrate-free and the two mono-glycosylated analogues are about equally active with bradykinin.

3. The double glycosylated derivative is about 5 times more potent than bradykinin.

4. All analogues have two different effects on synaptic transmission in the insect CNS—at first a direct and reversible block of excitatory nicotinic transmission with a concurrent activation of the inhibitory GABA-ergic system and, secondly, a delayed irreversible block of the transmission, comparable to the block described earlier for bradykinin and Thr⁶-bradykinin.

5. For the synaptic transmission in the insect CNS the double glycosylated kinin is about 5 times more potent than bradykinin.

1. Intracellular recordings were made from identified neurones in the visceral, (abdominal) ganglion of the snail, Helix aspersa. The hyperpolarising response of neurone E4 is a pure chloride event and has a reversal potential, (E_Cl), of −69.7 ± 1.7mV, (n = 4). This can be compared to depolarising responses of neurones E1 and E2 which are sodium mediated.

2. Four membrane transport system antagonists, all thought to affect trans-membrane chloride movement, were investigated with respect to the two different acetylcholine responses described.

3. Piretanide irreversibly blocks the hyperpolarising response in cell E4, (1–10 μM), increasing its inhibition with time but without changing E_Cl.

4. Furosemide irreversibly blocks both types of acetylcholine responses at concentrations in the nanomolar range; no change in E_Cl or E_Na was associated with the inhibition but the “passive” membrane resistance appeared to decrease. Inhibition increased with time, normally causing a significant effect after 10–30 min.

5. S.I.T.S. and ethacrynic acid appear very similar in effect; both reversibly block the two responses to acetylcholine and recovery after washing is virtually complete. The onset of antagonism is rapid and both compounds are slightly more effective against the hyperpolarising (“H”), response than the depolarising (“D”) response (threshold ∼10⁻⁵ M compared to ∼ 10⁻⁴ M). No change in E_Cl or E_Na was noted.

6. Piretanide and furosemide probably exert their effect by interactions with the neuronal cell membrane, disrupting the integrity of this structure, whereas S.I.T.S. and ethacrynic acid may interact more specifically with the acetylcholine receptor protein.

1. Cadmium induced metallothionein (MT) in crayfish hepatopancreas was measured by silver-saturation method.

2. An increase in MT content was recorded in crayfish hepatopancreas after 12 hr of exposure to 10 mg Cd/l.

3. There was found to be a linear relationship between MT concentrations in hepatopancreas and cadmium concentration in the water.

4. MT levels in hepatopancreas of 20 mg Cd/l exposed crayfish were 7-fold higher than those in control animals.

1. The effect of the protein kinase C (PKC) activators verrucosin B (VB), 1,2-sn-dioctanoylglycerol (diC₈) and phorbol-12-myristate-13-acetate (PMA), of arachidonic acid (AA) and of substances interfering with its release, re-uptake and metabolism was studied in Hydra vulgaris.

2. All PKC activators potently inhibited bud formation, VB and PMA being 10,000 × more potent than diC⁸. VB effect was maximal already after 10 min incubation with hydra and persisted at 24 hr incubations.

3. AA and substances inhibiting its re-uptake from cell membrane or its metabolism also inhibited bud formation, whereas oleyl-oxyethyl-phosphorylcholine (OOPC), an inhibitor of phospholipase A₂, potently induced bud formation.

4. The findings described herein suggest a role for both PKC activation and AA in the inhibition of bud formation in H. vulgaris.