524
Report and Abstracts
described on many occasions. The damage to the muscle fibres is associated with the hydrolysis of the plasma membrane . Regeneration begins with the activation of satellite cells at 248 hr, fusion of these cells to form myotubes at 48-72 hr and the subsequent maturation of the muscle fibres. This early regenerative response is not dependent upon innervation, but muscle growth subsequent to regeneration does not occur if the muscle is denervated . Pure myotoxic phospholipases do not appear to damage the microvasculature, and so haemorrhage is rare; muscle blood flow may actually be enhanced during early stages of regeneration . Most myotoxic venoms are isolated from elapid snakes, although some viperid and crotalid species are known to be myotoxic . Russell's viper is known to have caused muscle damage in victims of its bite in Sri Lanka, but muscle necrosis is not a problem in Thailand or Myanmar. Recent experimental work has confirmed that the venom of Sri Lankan forms of the snake is rich in phospholipase activity, and causes significant muscle damage in vivo and in vitro. Recovery is rapid. T)te venom of the Thai snake is only weakly myotoxic and although it causes severe haemorrhagic foci r» vivo, mùscle necrosis is not severe . The venom of the snake from central India, however, is moderately myotoxic, and ä15o potently haemorrhagic. Consequently, muscle damage is exceptionally severe, regeneration is poor, and in many cases, regenerated tissue is fibrotic and poorly organised. The combination of both haemorrhagc and myotoxic factors in a venom suggests that long-term damage to skeletal muscle is a probable outcome of an envenoming bite. Microbial toxins in foods. Y. Uaxo (Department of Toxicology and Microbial Chemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Ichigaya, Tokyo 162, Japan) . species of microbes belonging to fungi and algae produce toxic metabolites, mycotoxins and phycotoxins, and their contamination of foodstuffs causes food-borne poisoning and hazards to human health . Aflatoxin B, (AFB,) produced by a fungus Aspergillus flavus is one of the important natural contaminants, and its level in food is presumed to be closely associated with the incidence of human primary liver cancer in endemic areas. By the introduction of several biomarkers such as AF-albumin and AF-N7-guanine adducts and p53 suppressor gene, AFB, is now listed as a risk factor for human liver cancer, along with HBV. AFM a hydroxylated metabolite of AFB was detected in milk powder samples. This metabolite is also carcinogenic, and thus its residue gives rise to health hazards for infants. Trichothecenes such as nivalenol (NIV), deoxynivalenol (DON) and T-2 toxin (T-2), produced by Fusarium spp., contaminate cereals worldwide and induce moldy wheat poisoning in several wuntries . The trichothecenes are highly myotoxic to mammalian cells, immunotoxic and teratogenic. Their mutagenic and carcinogenic potentials are negative. By the introduction of rat medium-term bioassay with GST-P as a tumor marker, an enhancement of AFB,-initiated liver tumor in rats fed with NIV was demonstrated . Fumonisins produced by F. moniliforme are also hepatocarcinogenic and possess tumor-promoting activity . Its levels in corn are known to be associated with the incidence of esophageal cancer in endemic areas. HPLC-fluorometric analysis demonstrated its occurrence in corn, corn-based products and feeds produced in several Asian countries. Ochratoxin A (OTA) produced by various fungal genera is nephrotoxic and carcinogenic to kidneys. Its residues in human serum have been demonstrated by ELISA and HPLC analysis . Microcystins are one of phywtoxins produced by blue-green algae living in water. This phycotoxin exhibits tumor-promoting activity. In Shanghai areas, a close association between high incidence of human liver cancer and wnsumption of pond water was reported . It suggests an involvement of such microcystins in the induction of liver tumors. Highly sensitive, specific and inexpensive ELISA methods are newly developed in our laboratory for monitoring the environmental contaminants such as AFM, , OTA and microcystins. Their application will be summarized . VAR~ous
Ciguatera. M. F.
CADRA
(School of Life Science, Queensland University of Technology, Brisbane, Australia) .
poisoning occurs in humans after the ingestion of particular specimens of a variety of tropical marine fish and is caused by small quantities of potent polycyclic ether(s), ciguatoxin(s), the structure of which have only been elucidated in the past three years. Precursors of fish ciguatoxin are produced by the benthic dinoflagellate, Gambierdiscus toxicus, first described and linked to ciguatera in the late 1970x. The distribution of human ciguatera poisoning is confined mainly to the tropics where it is a considerable cause of morbidity. There have been many reports on the clinical manifestations and symptomatology of ciguatera poisoning. In general an initial gastrointestinal disturbance which may include nausea, vomiting, diarrhoea and abdominal pain is followed by neurological symptoms that may include paraesthesia, arthragia, myalgia, muscular paralysis, memory disturbance and temperature perception reversal . Cardiovascular changes including arrythmies and hypotension are also noted in some victims. Forty victims of a ciguatera outbreak in Australia in 1987 were followed over a 6-month period. Twenty-one of these victims still had at least one symptom after 6 months. Ciguatoxin has been shown to exert a fundamental action on voltage dependent Na+ channels . In our laboratory the actions of ciguatoxin have been assessed on a variety of peripheral nerve preparations in rats, humans and fish . These electrophysiological studies have shown a slowing of conduction velocity, the prolongation of refractory periods and an CticuA~retu