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236 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

235.15 Ų [M]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

White to light-tan crystalline alkaloid; odorless. MP 270 °C with decomposition. Soluble in water and alcohol; insoluble in acetone, chloroform, and ether; aqueous solution is strongly dextrorotary (specific rotation for 1% solution of anhydrous -208 to +218 degrees). /Chloride/

ODORLESS, WHITE, YELLOWISH WHITE TO GRAYISH WHITE CRYSTALLINE POWDER /CHLORIDE/

ODORLESS, WHITE OR PALE YELLOW CRYSTALLINE POWDER /DIMETHYL IODIDE/

CRYSTALS; MAX ABSORPTION: 280 NM (E= 74, 1%, 1CM); SOL IN WATER APPROX 300 MG/100 ML; SLIGHTLY SOL IN DIL HYDROCHLORIC ACID, DIL SODIUM HYDROXIDE; VERY SLIGHTLY SOL IN ALC; PRACTICALLY INSOL IN BENZENE, ETHER, CHLOROFORM; SPECIFIC OPTICAL ROTATION: +148 TO +158 DEG @ 22 °C/D (0.25%) /DIMETHYL IODIDE/

SPECIFIC OPTICAL ROTATION: +190 DEG @ 22 °C/D (0.5%); +219 DEG @ 23 °C/D (METHANOL, 0.785%); DECOMP APPROX 270 °C /PENTAHYDRATE, CHLORIDE/

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

Tubocurarine is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Large doses and overdoses may cause respiratory paralysis and hypotension.

Inadvertent intraarterial injection of tubocurarine in the left antecubital fossa results in pain and weakness of the extremity. /Tubocurarine chloride/

ANIMALS POISONED BY D-TUBOCURARINE ... 1ST EXHIBIT MOTOR WEAKNESS, & ULTIMATELY MUSCLES BECOME TOTALLY FLACCID & INEXCITABLE ... MUSCLES ... OF FINGERS, TOES, EYES, & EARS ARE INVOLVED BEFORE THOSE OF LIMBS, NECK, & TRUNK. ULTIMATELY INTERCOSTAL MUSCLES & FINALLY DIAPHRAGM ARE PARALYZED, & RESP THEN CEASES.

DEATH /IN ANIMALS POISONED BY D-TUBOCURARINE/ IS CAUSED BY HYPOXIA SECONDARY TO PERIPHERAL RESPIRATORY PARALYSIS. TERMINAL ASPHYXIAL CONVULSIONS MAY APPEAR, BUT THESE ARE MILD OWING TO ALMOST COMPLETE MUSCULAR PARALYSIS.

SALIVATION, RETCHING, DEFECATION, BRONCHOSPASM, & INTESTINAL HEMORRHAGE REPORTED IN DOGS ARE PROBABLY IN PART ASSOC WITH.../D-TUBOCURARINE'S/ HISTAMINE RELEASE. /CHLORIDE/

HYPOTHERMIA ANTAGONIZES D-TUBOCURARINE-INDUCED NEUROMUSCULAR BLOCKADE BUT DECR ELIMINATION. AT 28 DEGREE NET EFFECT IS PROLONGATION OF NEUROMUSCULAR BLOCKADE.

For more Non-Human Toxicity Excerpts (Complete) data for TUBOCURARINE (7 total), please visit the HSDB record page.

LD50 Rat ip 210 ug/kg

LD50 Rat im 500 ug/kg

LD50 Mouse ip 410 ug/kg

LD50 Mouse sc 560 ug/kg

For more Non-Human Toxicity Values (Complete) data for TUBOCURARINE (9 total), please visit the HSDB record page.

AFTER IV ADMIN OF (3)H-D-TUBOCURARINE TO DOGS, 36% OF (3)H WAS EXCRETED IN URINE IN 3 HR & 75% IN 24 HR. KINETICS INDICATED THAT RENAL EXCRETION OCCURRED BY GLOMERULAR FILTRATION, & AS THERE WOULD BE NEGLIGIBLE TUBULAR REABSORPTION FOR THIS POORLY LIPID-SOL, IONIZED DRUG, ELIMINATION WAS RAPID.

Up to two-thirds of an administered dose of tubocurarine is excreted in the urine over a period of several hours; smaller quantities appear in the bile, and a variable amount is metabolized. Insignificant amounts of tubocurarine cross the placenta.

The brief duration of paralysis following the initial dose is due to redistribution of the drug; when repeated doses are administered, the tissues become saturated and factors of degradation and excretion then directly influence intensity and duration of action.

INITIAL APPARENT VOLUME OF DISTRIBUTION OF TUBOCURARINE WAS APPROX SAME AS SERUM VOLUME & APPEARED TO INCR WITH SIZE OF DOSE. FRACTION OF DOSE WAS DISTRIBUTED IN NON-VASCULAR SPACES OR BOUND TO TISSUE @ LARGER DOSES.

For more Absorption, Distribution and Excretion (Complete) data for TUBOCURARINE (9 total), please visit the HSDB record page.