Intoxication oral intoxications

Biological considerations Orally, will produce transient neurobehavioral intoxication. Oral LD50 (rats)= 13.0 mlkg-1. Intravenous LD50 (mice) = 5.1 ml kg 1... 

The neurotoxins may be transmitted to man through bioaccumulation in an intermediate marine host. Toxic bivalves result from the filter-feeding of jP. brevis cells during red tides, and if consumed result in neurotoxic shellfish poisoning, or NSP. Human oral intoxication is rarely fatal. 

Acute oral intoxication is characterized by an initial phase in which gastrointestinal effects such as nausea and vomiting predominate, followed by an apparent recovery period lasting up to 2 days, which in turn is followed by the return of gastrointestinal symptoms plus... 

Adverse effects consist mainly of gastrointestinal intolerance such as nausea, epigastric pain and diarrhea and, especially in the elderly constipation with continued therapy. All ferrous salts may cause a black coloration of the faeces. Children are particularly susceptible to potentially lethal iron intoxications. Oral iron preparations should not be administered concurrently with tetracyclines as mutual interference with absorption will occur. 

Muller G, Bemuzzi V, Desor D, et al. 1990. Developmental alterations in offspring of female rats orally intoxicated by aluminum lactate at different gestation periods. Teratology 42 253-261. 

Muller G, Bumel D, Gery A, et al. 1993a. Element variations in pregnant and nonpregnant female rats orally intoxicated by aluminum lactate. Biol Trace Elem Res 39 211-219. 

In addition to nonhuman primates, most other animal species that show some sensitivity to botulinum intoxication are in fact susceptible to toxin serotypes Cl and D. Several rodent species are susceptible to oral intoxication with most botulinum toxins, including types Cl and D (Matveev, 1959 ... 

The administration of heterologous antitoxin was one of the first therapeutic approaches developed for botuhsm patients and remains the most effective when initiated in the early stages of intoxication. The primary limitation of antitoxin treatment was established in some of the earhest published reports on experimental botuhsm. One of these reports evaluated the pathogenesis of oral intoxication and the efficacy of antitoxin therapy in monkeys (Back and Wood, 1928). Antitoxin treatment was not effective when administered after symptoms of botulism were already apparent, despite the fact that circulating toxin could still be detected in many of the animals. 

We might turn an argument around to substantiate the hypothesis that, especially in acute oral intoxications, the animals do not die from the toxin but from secondary effects to the GIT It has been documented in at least three major attempts, that cytotoxicity correlates pretty well with acute oral toxicity (see Halle register, MEIC study and the more recent ICCVAM/NICEATM/ECVAM validation study). Actually, this makes little sense if we assume that the substances are taken up, distributed and metabolized with complex kinetics and can affect more than 400 different tissues with various sensitivities. Might it be that the animal experiment simply measures cytotoxicity to the GIT epithelium, which results in translocation of bacteria Ironically, this would mean that we can pretty well predict this animal test in vitro, because the animal test measures a phenomenon (cytotoxicity to the intestine) that is irrelevant for humans (we would vomit—which rodents cannot do—or remove the intoxication before it reaches the intestine, supply intensive care treatment, etc.). Instead of our 9 million effort of A-Cute-Tox (http //www.acutetox.org/), a well-designed series of animal experiments might demonstrate that the reference method is meaningless. 

The primary concern after oral intoxication with formaldehyde is correcting the severe acidosis and decreased blood pressure that this chemical induces. Treatment should aimed at increasing the blood pressure to a somewhat normal state (sympathomimetic drugs may be used) as well as treating the acidosis with bicarbonate (Aaron and Howland 1994 Gossel and Bricker 1994). Dialysis may also be used to remove excess formate (as formic acid) in the blood in order to correct the acidosis (Burkhart et al. 1990 Eells etal. 1981). 

Saxitoxin, the best known example of this group, is a potent neurotoxin found in shellfish such as mussels, clams, and scallops. Saxitoxin is a sodium channel-blocking agent and is more toxic by inhalation than by other routes of exposure. Unlike oral intoxication with saxitoxin (paralytic shellfish poisoning), which has a relatively slow onset, inhala-tional intoxication with saxitoxin can be lethal in a few minutes. Saxitoxin could be used against our troops as an antipersonnel weapon, but because it cannot currently be chemically synthesized efficiently, or produced easily in large quantities from natural sources, it is unlikely to be seen as an area aerosol weapon on the battlefield. 

Trichothecene Mycotoxins. Only one class of easily produced, membrane-damaging toxins, the trichothecene mycotoxins, is dermally active. Therefore, they must be considered by standards different from those for all other toxins. Trichothecenes can cause skin lesions and systemic illness without being inhaled and absorbed through the respiratory system. Skin exposure and ingestion of contaminated food are the two likely routes of exposure of soldiers oral intoxication is unlikely in modern, well-trained armies. Nanogram quantities per square centimeter of skin cause irritation, and microgram quantities cause necrosis. If the eye is exposed, microgram doses can cause irreversible injury to the cornea. 

CLINICAL SYMPTOMS, SIGNS, AND PATHOLOGY Oral Intoxication Injection Inhalation Cause of Death... 

As is the case in toxicity and pathogenesis of intoxication, the route of exposure is important in relation to possible modes and their likelihood of success of prophylaxis and therapy. For oral intoxication, supportive therapy includes activated charcoal administration and intravenous fluid and electrolyte replacement. For inhalational intoxication, supportive therapy to counteract acute pulmonary edema and respiratory distress is indicated. Symptomatic care is the only intervention presently available to clinicians for the treatment of incapacitating or lethal doses of inhaled ricin. Positive end-expiratory ventilatory therapy, fluid and electrolyte replacement, antiinflammatory agents, and analgesics... 

For the detoxification of electrolytes taken in an overdose, for the most part other rules have to be followed. For example, it is recommended that oral intoxications with Mg be treated with hemodialysis and Ca [81]. This is also an example for the application of antagonistic metals in the therapy of metal intoxication. 

Koseoglu Z, Satar S, Kara B, Sebe A, Kosenli O. An unusual case of mesalazine intoxication oral and rectal overloading of the rectal suppository form. Hum Exp Toxicol 2011 30 772-6. 

Mahieu P, Buchet J-P, Lauwerys R (1987) Evolution clinique et biologique d une intoxication orale aigue par Tanhydride arsenieux et considerations sur I attitude therapeutique. J Toxicol Clin Exp 7 273-278 Maiorino RM, Aposhian HV (1985) Dimercaptan metal-binding agents influence the biotransformation of arsenite in the rabbit. Toxicol Appl Pharmacol 77 240-250 Marafante E, Vahter M (1984) The effect of methyltransferase inhibition on the metabolism of As]arsenite in mice and rabbits. Chem Biol Interact 50 49-57... 

Simpson, 1998). The authors speculated that since human tissues are fully sensitive to the neuromuscular blocking properties of Cl neurotoxin (Coffield et al., 1997 Eleopra et al., 2004), the relative absence of human foodbome type C botulism could be due to the inability of this toxin to penetrate from the gut to the general circulation. Human susceptibility to type Cl and D neurotoxins remains unclear however, clarification of this issue will be important in interpreting data derived both from in vitro studies on toxin transcytosis and from animal models for oral intoxication. 

Oral Intoxication Toxin Absorption from the Gastrointestinal Tract... 

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. 

Poly(vinyl alcohol) has a low oral toxicity rating. The oral LD q is higher than 10,000 mg/kg (rats). Concentrations of up to 10,000 mg/L in water were tested for toxicity to bluegik sunfish. No mortaUty or response indicative of intoxication was observed (283). 

Humans tolerate fairly large oral doses of copper without harmful effects, and it is used in various therapies (66). Copper sulfate is a powerful emetic and has been used clinically in the treatment of intoxications. 

Bccesave dosage is manifested as water intoxication (fluid overload). Symptoms of water intoxication include drowsiness, listlessness confusion, and headache (which may precede convulsions and coma). If sgns of excessive dosage occur, the nurse should notify the primary health care provider before the next dose of the drug is due because a change in the dosage, the restriction of oral or IV fluids and the administration of a diuretic may be necessary. 

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