saxitoxin and Muscle-Weakness

Saxitoxins (STX) and tetrodotoxins (TTX) are a group of chemical compounds produced by certain species of marine algae and fish. Lethal dose for a human is about 0.5-2.0 mg when the toxin enters the body via food, and 0.05 mg of poisoning at the time of injection. In the case of aerosol the lethal dose for human being is 5 mg/min/m(3). STX and TTX poisoning cause mostly symptoms from the nervous system in the form of: paresthesia around the lips, tongue, gums, distal segments of the limbs, headache, dysphonia, astigmatism, floating feeling, muscle weakness, paralysis of cranial and peripheral nerves. There is no specific antidote for STX and TTX. It is recommended supportive treatment.

Topics: Administration, Inhalation; Administration, Oral; Aerosols; Animals; Astigmatism; Biological Warfare Agents; Dysphonia; Headache; Humans; Lethal Dose 50; Muscle Weakness; Paralysis; Paresthesia; Saxitoxin; Tetrodotoxin

Muscle weakness and aberrant responses to neuromuscular relaxants after burn injury are associated with upregulation of acetylcholine receptors (AChRs). Typically, these functional, pharmacological, and biochemical changes occur after denervation, in which transcriptionally mediated qualitative changes in AChRs and Na+ channels and of myogenic regulatory proteins MyoD and myogenin also occur. This study in rats, by an examination of changes in the above-enumerated proteins or their transcripts in the gastrocnemius muscle distant from the burn, verifies whether a denervation-like state exists after burns. Scatchard analysis of [3H]saxitoxin binding revealed no changes in the affinity (K(d)) and total number (B(max)) of Na+ channels between control and burn-injured animals at both 7 and 14 days after injury. The mRNA levels of the immature proteins, SkM2 of the Na+ channels and the gamma-subunits of AChRs, the increase of which is pathognomic of denervation, were assessed by Northern analysis and were unchanged. The transcripts of mature Na+ channels, SkM1, were significantly increased at day 14 after the burn (1.24 +/- 0.10 in burn-injured vs. 1.06 +/- 0.12 in sham animals, arbitrary units, P = 0.006). Although MyoD levels were increased in burn-injured animals at 14 days (0.21 +/- 0.02 vs. 0.15 +/- 0.07 arbitrary units, P = 0.05), myogenin levels were unaltered. The absence of changes in AChR transcripts, including alpha-, delta-, and gamma-subunits, indicates that the upregulation of AChR in burns is not transcriptionally mediated. The unaltered levels of transcripts of myogenin, SkM2 of Na+ channels and gamma-subunit of AChR, confirm that there is no denervation-like prejunctional (nerve-related) component to explain the muscle weakness or the upregulation of AChRs at sites distant from burns.

Topics: Animals; Blotting, Northern; Body Weight; Burns; Male; Muscle Denervation; Muscle Weakness; Muscle, Skeletal; Rats; Rats, Sprague-Dawley; Receptors, Cholinergic; RNA; Saxitoxin; Sodium Channels; Up-Regulation