Muscle poisons

Muskel-. muscular, myo-, -eiweiss, n, myosin, -empfindung, /, muscular sensation, -farb-stoff, m. muscle pigment, -faser,/, muscular fiber, -fleisch, n, muscular substance, -ge-webe, n. muscular tissue, -gift, n, muscle poison, -lehre, /, myology, -masse, /. muscular substance, -saft, m. muscle juice,. -stoff, m. sarcosine. -zucker, m. inositol. Muskowit, Muskovit, m. (Min.) muscovite, muss, pr. 1 tS 3 sing, (of miissen) must. 

Barium ion is a muscle poison causing stimulation and then paralysis. Initial symptoms are gastrointestinal, including nausea, vomiting, colic, and diarrhea, followed by myocardial and general muscular stimulation with tingling in the extremities. Severe cases continue to loss of tendon reflexes, general muscular paralysis, and death from respiratory arrest or ventricular fibrillation. Threshold of a toxic dose in humans is reported to be about 0.2-0.5 g Ba absorbed from the gut the lethal dose is 3 g Ba. 

Rabuteau7 claims that all potassium salts are muscle poisons. When injected into the veins of a dog, death occurred with low concentrations of potassium salts and no effect with much higher concentrations of sodium salts. Some of Rabuteau s data are given in Table 1. 

In terms of their mode of action, insecticides fall into seven classes physical toxicants, protoplasmic poisons, nerve poisons, metabolic inhibitors, cytolytic toxins, muscle poisons, and alkylating agents. 

Brown GB (1988) Batrachotoxin a window on the allosteric nature of the voltage-sensitive sodium channel. Int Rev Neurobiol 29 77-116 Brunton L, Cash T (1883) Influence of heat and cold upon muscles poisoned by veratria. J Physiol (Lond) 4 1-17... 

The heart poisons or cardiotoxins are, in reality, general muscle poisons. However their effect on the muscle of the heart is by far the most important in terms of killing the snake s prey or attacker. These incredibly potent toxins bind to specific biochemical sites on the surface of muscle cells causing depolarisation. The muscle cell works in a manner akin to neurones in that it transmits information, to initiate a contraction, by exchanging + and - ions across its cell... 

While Ling studied the Na efflux of frog muscle at 0°C, Keynes, Maisel, and Conway et al. studied Na efflux at room temperature. In Ling s work, the absence of change in the Na" efflux rate was shown to accompany a maintained low level of Na and high level of K in the muscle cells. The level of Na" " and K in frog muscle poisoned at room temperature with lAA and other metabolic poisons was not reported by either Keynes and Maisel or Conway et al. If they did, they would have noticed... 

Important toxins are cobramine A and B from cobra toxin and crotactine and crotamine from crotox-in, the toxin of the North American rattlesnake. The toxic proteins are classified according to their mode of action cardiotoxins, neuFotoxins and protease inhibitors (with inhibitory activity toward chymotrypsin and trypsin). Cardiotoxins (heart muscle poisons) cause an irreversible depolarization of the cell membranes of heart muscle and nerve cells. Neurotoxins (nerve poisons) show curare-like activity they prevent neuromuscular transmission by blocking the receptors for the transmitters at the synapses of autonomic nerve endings and at the motor end plate of skeletal muscle. Protease inhibitors inhibit acetylcholine esterase and similar enzymes involved in nerve transmission. 

He worked on the sources of energy for muscular contraction, a continuation of his first interest in muscle creatine. Phosphagen had been recently discovered. Einar Lundsgaard had just shown that muscle poisoned with iodoacetic acid was able to perform a certain amount of work without liberation of lactic acid. Using muscles with low carbohydrate content, Ochoa was able to demonstrate the muscle s ability to perform work using sources of energy different from those then known. It was an important piece of work on a topic of great interest at the time. 

Muscle poisons. Affect the muscles, causing muscle weakness and loss of function. Some substances affect smooth (involuntary) muscle. Example barium salts. Some affect cardiac muscle, producing cardiac arrhythmias, angina, and muscle weakness. Examples nicotine, halogenated hydrocarbons, carbon monoxide, potassium salts, nitrates. Cardiovascular poisons can cause coronary artery disease and hypertension. Example carbon disulfide (80). 

Rya.nia., The root and stem of the plant yania speciosa family Flacourtiaceae, native to South America, contain from 0.16—0.2% of iasecticidal components, the most important of which is the alkaloid ryanodine [15662-33-9] C25H250 N (8) (mp 219—220°C). This compound is effective as both a contact and a stomach poison. Ryanodine is soluble ia water, methyl alcohol, and most organic solvents but not ia petroleum oils. It is more stable to the action of air and light than pyrethmm or rotenone and has considerable residual action. Ryania has an oral LD q to the rat of 750 mg/kg. The material has shown considerable promise ia the control of the European com borer and codling moth and is used as a wettable powder of ground stems or as a methanohc extract. Ryanodine uncouples the ATP—ADP actomyosia cycle of striated muscle. 

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Barium metal and most barium compounds are highly poisonous. A notable exception is barium sulfate which is nontoxic because of its extreme iasolubihty ia water. Barium ion acts as a muscle stimulant and can cause death through ventricular fibrillation of the heart. Therefore, care must be taken to avoid contact with open areas of the skin. Workers must wear respirators (of type approved for toxic airborne particles), goggles, gloves, and protective clothing at all times. The toxic barium aluminate residue obtained from barium production is detoxified by reaction with a solution of ferrous sulfate and converted iato nontoxic barium sulfate. According to OSHA standards, the TWA value for Ba and Ba compounds ia air is 0.5 mg/m. ... 

Benzene is a flammable liquid and its vapors are toxic and explosive. Low concentrations are dangerous on continued inhalation because benzene affects the blood forming function of the bone marrow and it is a cancirogen. Dermatitis may result from repeated skin contact. Alkyl derivatives such as toluene and xylenes are far less toxic and are, therefore, much safer than benzene for use in solvents. Some of the symptoms of benzene poisoning are dizziness, constriction of the chest, and tightening of the leg muscles. 

PuAEMACoLOGiCAL AcTiox. Curare is stated to be almost inert when taken by mouth, owing to poor absorption by intestinal mucous membrane and the rapidity of elimination. Injected hypodermically it is a rapid and potent poison, paralysing the motor nerve-endings in striped muscle, so that voluntary movements cease and death occurs from respiratory failure. 

Brucine closely resembles strychnine in action, but is much less poisonous and it also has a more marked curare-like action on the nerve-endings in voluntary muscle. 

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

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