Sea nettle (Chrysaora quinquecirrha) nematocyst venom: mechanism of action on muscle.
The cellular mechanism of toxicity of sea nettle nematocyst venom was studied in the isolated, perfused frog ventricle and the isolated frog sartorius muscle. The venom depolarized both cardiac muscle fibers and sartorius fibers and shortened the duration of the ventricular action potential. Sodium content was increased, potassium content was decreased and magnesium content was unaltered in both tissues upon exposure to venom. Calcium content increased in heart ventricle, twitch tension decreased and a contracture developed. The calcium content of venom-treated, quiescent sartorius muscles was not changed from control. In stimulated sartorius muscles, tetanus tension fell during venom treatment, the twitch response was variable and no contracture was seen. Venom-treated sartorius muscles incubated with 5 mM Rb+, Cs+ or Li+ took up twice the amount of each cation as did control muscles. Sea nettle venom decreased the resistance of black lipid membranes in discrete steps, each step corresponding to a transfer of about 2 X 10(7) ions/sec at a potential of 20 mV in Ringer's solution. It was concluded that a component of sea nettle venom forms a monovalent cation channel in cardiac skeletal muscle surface membranes that allows a rapid influx of sodium into the cell.
D000818:Animals; D002462:Cell Membrane / Q000187:drug effects; D004573:Electrolytes / Q000032:analysis; D005397:Fish Venoms / Q000633:toxicity*; D007473:Ion Channels / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000187:drug effects*; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000032:analysis; D011894:Rana pipiens; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D004573:Electrolytes; D005397:Fish Venoms; D007473:Ion Channels; D012964:Sodium; D012413:Rubidium