In high doses,<unk>  is very toxic to humans (minimum lethal oral dose in adults is 30–120 mg) and many other animals (oral = 16 mg/kg in rats, 2 mg/kg in mice), and poisoning by inhalation, swallowing, or absorption through eyes or mouth can be fatal. S. nux-vomica seeds are generally effective as a poison only when they are crushed or chewed before swallowing because the pericarp is quite hard and indigestible; poisoning symptoms may therefore not appear if the seeds are ingested whole. Animal toxicity<unk>  poisoning in animals usually occurs from ingestion of baits designed for use against gophers, moles, and coyotes.<unk>  is also used as a rodenticide, but is not specific to such unwanted pests and may kill other small animals. In the United States, most baits containing<unk>  have been replaced with zinc phosphide baits since 1990. In the European Union, rodenticides with<unk>  are forbidden since 2006. Some animals are immune to<unk> , usually these are species such as fruit bats that have evolved resistance to poisonous alkaloids in the fruit they eat. The drugstore beetle has a symbiotic gut yeast that allows it to digest pure<unk> .<unk>  toxicity in rats is dependent on sex. It is more toxic to females than to males when administered via subcutaneous injection or intraperitoneal injection. Differences are due to higher rates of metabolism by male rat liver microsomes. Dogs and cats are more susceptible among domestic animals, pigs are believed to be as susceptible as dogs, and horses are able to tolerate relatively large amounts of<unk> . Birds affected by<unk>  poisoning exhibit wing droop, salivation, tremors, muscle tenseness, and convulsions. Death occurs as a result of respiratory arrest. The clinical signs of<unk>  poisoning relate to its effects on the central nervous system. The first clinical signs of poisoning include nervousness, restlessness, twitching of the muscles, and stiffness of the neck. As the poisoning progresses, the muscular twitching becomes more pronounced and convulsions suddenly appear in all the skeletal muscles. The limbs are extended and the neck is curved to opisthotonus. The pupils are widely dilated. As death approaches, the convulsions follow one another with increased rapidity, severity, and duration. Death results from asphyxia due to prolonged paralysis of the respiratory muscles. Following the ingestion of<unk> , symptoms of poisoning usually appear within 15 to 60 min. The LD50-values for<unk>  in animals are listed below in table 1. The LD50 values for<unk>  in animals Organism Route LD50 (mg/kg) Bird-wild Oral 16 Cat Intravenous 0.33 Cat Oral 0.5 Dog Intravenous 0.8 Dog Subcutaneous 0.35 Dog Oral 0.5 Duck Oral 3.0 Mouse Intraperitoneal 0.98 Mouse Intravenous 0.41 Mouse Oral 2.0 Mouse Parenteral 1.06 Mouse Subcutaneous 0.47 Pigeon Oral 21.0 Quail Oral 23.0 Rabbit Intravenous 0.4 Rabbit Oral 0.6 Rat Oral 16.0 Rat Intravenous 2.35 Human toxicity An 1809 painting depicting opisthotonus After injection, inhalation, or ingestion, the first symptoms to appear are generalized muscle spasms. They appear very quickly after inhalation or injection – within as few as five minutes – and take somewhat longer to manifest after ingestion, typically approximately 15 minutes. With a very high dose, the onset of respiratory failure and brain death can occur in 15 to 30 minutes. If a lower dose is ingested, other symptoms begin to develop, including seizures, cramping, stiffness, hypervigilance, and agitation. Seizures caused by<unk>  poisoning can start as early as 15 minutes after exposure and last 12–24 hours. They are often triggered by sights, sounds, or touch and can cause other adverse symptoms, including hyperthermia, rhabdomyolysis, myoglobinuric kidney failure, metabolic acidosis, and respiratory acidosis. During seizures, mydriasis (abnormal dilation), exophthalmos (protrusion of the eyes), and nystagmus (involuntary eye movements) may occur. As<unk>  poisoning progresses, tachycardia (rapid heart beat), hypertension (high blood pressure), tachypnea (rapid breathing), cyanosis (blue discoloration), diaphoresis (sweating), water-electrolyte imbalance, leukocytosis (high number of white blood cells), trismus (lockjaw), risus sardonicus (spasm of the facial muscles), and opisthotonus (dramatic spasm of the back muscles, causing arching of the back and neck) can occur. In rare cases, the affected person may experience nausea or vomiting. The proximate cause of death in<unk>  poisoning can be cardiac arrest, respiratory failure, multiple organ failure, or brain damage. The minimum lethal dose values estimated from different cases of<unk>  poisoning are listed below in table 2. Minimum lethal dose estimates for<unk>  in humans Route Dose (mg) Human Oral 100–120 Human Oral 30–60 Human (child) Oral 15 Human (adult) Oral 50–100 Human (adult) Oral 30–100 Human Intravenously 5–10 (approximate) For occupational exposures to<unk> , the Occupational Safety and Health Administration and the National Institute for Occupational Safety and Health have set exposure limits at 0.15 mg/m3 over an 8-hour work day. Because<unk>  produces some of the most dramatic and painful symptoms of any known toxic reaction,<unk>  poisoning is often portrayed in literature and film including authors Agatha Christie and Arthur Conan Doyle.
Strychnine
Cromoglicic acid
Deoxypyridinoline
Pyridinoline
Phenibut
Thiotepa
Charybdotoxin
Beta-Zearalenol