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Report and Abstracts
by i.p. injecting into mice. In order to calibrate the test, a 'standard symptoms scale' was made from 0 (no effect) to 5 (death). Various in vitro toxicity tests were carried out on the previously described extracts. The toxicity against a variety of cells, such as sheep red blood cells (normal), hepatocytes (normal), KB cells (proliferative), sea urchin eggs (embryonic) and bacteria, was evaluated. The effects on isolated frog heart were measured. Three conclusions result from these studies: (1) none of these activities was directly related to the acute toxicity on mice; (2) no hepatotoxicity was observed; and (3) there seems to be an inverse relation between the cytotoxicity on KB cells and the acute toxicity.
Effects ofpenitrem A on learning in rats. O. Deschaux, J. C. Bizot, P. Breton, J. Buee and I. De La Manche (Laboratoire de Pharmacologie du Comportement, Centre d'Etudes du Bouchet, BP 3. 91710 Vert-le-Petit, France). Penitrem A (PA) is a mycotoxin isolated from Penicillium palitans. Administered i.p. to rats, it induces dose-related symptoms, from slight tremors and limb weakness at low doses (0.2 and 0.4 mg/kg) to sustained tremors, ataxia, convulsions and death at higher doses (0.8 2 mg/kg). It has been claimed that PA can act as a partial agonist of GABA receptors (Selala et al., 1989). Since there is substantial evidence to show that GABA plays an important role in learning and memory processes, we attempted to determine the effect of PA in two learning tasks in rats. The passive avoidance test took place in a box consisting of a large lighted compartment and a small dark one with a grid floor connected to an electric shock provider. During the training trial, the rat was placed in the lighted compartment. As soon as it entered into the dark compartment, an electric foot shock was delivered, then the rat was removed from the apparatus and replaced in the home cage. The retention test, given 24 hr later, was conducted as above except that no electric foot shock was applied. The time taken by the rat to re-enter the dark compartment (called step-through latency) was recorded up to a maximum of 180sec. PA (0.2 and 0.4mg/kg) administered 30min before the training trial significantly reduced the step-through latency. PA (0.4 mg/kg) administered l0 or 20 min before training or 30 min before the retention test had no effect. Physostigmine, an acetylcholinesterase (ACHE) blocker, and bicuculline, a blocker of GABA A receptors, did not antagonize the disruption induced by PA (0.4 mg/kg). Morris water maze test took place in a circular pool filled with water made opaque with milk. An escape platform was set always at the same place in the pool. It was submerged 1 cm below the water surface, making it invisible from water level. The experiment consisted of two sessions of nine trials separated by 1 day. For each trial, the rat was placed in the water always at the same place and the time taken to find the platform was measured. The learning of this task was assessed by the decrease of this parameter during trials of the first session and between the second and the first session. PA (0.4 mg/kg) administered 30 min before the first session disrupted learning. Administered at the same dose to well-trained animals, PA did not significantly disrupt their ability to find the platform. Taken together, these results indicate that PA impairs the learning but not the retrieval of two tasks: passive avoidance and spatial. This effect does not seem to be due to a disruption of memory consolidation, since administration of PA 10 or 20 min before learning of passive avoidance, so that it acts just after learning, had no effect. Moreover, the absence of antagonism of the passive avoidance deficit by physostigmine and bicuculline indicates that cholinergic pathways and GABA a receptors are not involved in PA-induced learning impairment. Selala et al. (1989) Drug chem. Toxic. 12, 237 257.
Stud), o f Scorpaena scrofa and Scorpaena porcus venom: the preliminaries o f a qualitative analysis. R. Eon-Gerhardt (Laboratory of Cellular Biology, U F R Pharmacie, 35 Chemin des Maraichers, 31062 Toulouse, France). The venom apparatus of the scorpion fish has been extensively studied by Physalix (1922), Pawlovsky (1906, 1909), Halstead (1956, 1971), and Lagraulet et al. (1982). The toxicity of the venom was mainly proved by Dunbar Brunton (1896), Briot (1904, 1905), Physalix (1922, 1931), Lumiere and Meyer (1938), Halstead (1956, 1971), Maretic (1957, 1980), Lagraulet (1972, 1982), and Russell (1975). According to a procedure similar to that of Lagraulet, who showed by electrophoretic analysis that the proteins of the venom had a tool. wt between 10 and 1000 kDa, we tried to carry out a qualitative study on some non-dialysed venom. Extracts of the whole venom apparatus (pelvic, anal, dorsal) were obtained from freshly caught scorpion fish, to evaluate the protein composition and to highlight the variations between different species, for similar toxic effects. Furthermore, we could confirm, after mice dissection, the neurotoxic effects of the venom and its consequence on the heartbeat, after i.v. or i.p. injections. We have developed a method of extracting the venom at a low temperature (4°C) to prevent protein instability, and used a technique of PAGE natif (Phast gel Pharmacia from 4% to 15%) for protein analysis. Our results show that there are no significant similarities between the proteins in the venom extract from Seorpaena scrofa and those extracted from Scorpaena porcus.