Neurotoxicity poisoning from

FIGURE 69.3. In vitro protection of AChE from inhibition hy paraoxon or DFP by enzymatic hioscavengers (OPH or OPAA) and 2-PAM. The P50 value is the ratio at which 50% of a fixed concentration of AChE is protected from neurotoxic poisoning. From left to right, the kinetic curves are (1) OPH and paraoxon (2) OPH and DFP (3) OPAA and DFP (4) 2-PAM and paraoxon (5) 2-PAM and DFP (6) OPAA and paraoxon. 

Chronic effects of arsenic poisoning include neurotoxic effects to the central and peripheral nervous systems. Symptoms include sensory changes, muscle sensitivity, prickling and tingling sensations (paresthesia), and muscle weakness. Liver injury is a common symptom of chronic arsenic poisoning. Studies of victims of chronic arsenic poisoning from contaminated drinking... 

Neurotoxic poisoning can result in five different categories of indicators. These and their symptoms are presented in Table 18.3. The material presented in Table 18.3 and the format has been adapted from the... 

Solomon LM, Fahrner L, West DP (1977) Gamma benzene hexachloride toxicity a review. Arch Dermatol 113 353-357 Spencer PS, Bischoff MC (1987) Skin as an entry for neurotoxic substances. In Marzulli FN, Maibach HI (eds) Dermatotox-icology. Hemisphere, New York, pp 625-640 Stanley BE, Frank JE (1971) Mercury poisoning from application to omphalocele. JAMA 216 2144-2145 Steele CE, Trasler DG, New DA (1983) An in vivo/in vitro evaluation of the teratogenic action of excess vitamin A. Teratology 28 209-214... 

The toxicological consequences of P. brevis red tides are mass mortality of fishes exposed to the red tide toxic shellfish which, if consumed, result in human neurotoxic shellfish poisoning and an irritating aerosol which results from contact with P. brevis cell particles entrapped in seaspray. In all cases, the threshhold levels for intoxication are in the picomolar to nanomolar concentration ranges, implying a specific locus or loci of action for brevetoxins (reviewed in 6). 

In general, the clinical presentation of the human diseases associated with the ingestion of marine seafood toxins is similar to that of any other food poisoning disease. However, a number of clinical issues make these diseases particularly difficult to diagnose and treat. For example, the neurotoxic syndromes associated with CFP, PSP, and NSP represent points along a continuum of disease severity rather than clinically exclusive diseases. Even if fish or other seafood is the suspected source of a disease outbreak, diarrhea associated with the outbreak could be misdiagnosed as originating from bacterial rather than from phycotoxin contamination. 

Paralytic shellfish poison, like botulinum toxin, is a neurotoxic substance and can also affect certain muscles, including the heart, which are under nervous system control. Some poisoned humans who have recovered from the effects of PSP have described the early stages of intoxication as not at all unpleasant a tingling sensation in the lips and face and a feeling of calm. Those who die from PSP ingestion do so because of respiratory failure. 

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. 

Earlier research had already suggested that certain blooms Aph. flos-aquae could produce paralytic shellfish poisons. These studies used water blooms collected from Kezar Lake, New Hampshire (25,30). In 1980 Carmichael isolated a neurotoxic strain of Aph. flos-aquae from a small pond in New Hampshire. These strains have also been shown to produce toxins similar to saxitoxin and neo- axitoxin (23) and are the ones used in the studies presented here. 

The puffer fish is probably the best known neurotoxic fish. Several related species of fish, as well as other marine life, such as some frogs, starfish, octopus, and others, contain tetrodotoxin. Many people consider this fish a delicacy despite the occasional death from poor preparation. Tetrodotoxin is heat stable but water soluble, so careful preparation is necessary to limit neurological effects. Symptoms of poisoning include a rapid onset of numbness in the lips and mouth, which then extends to the fingers and toes, followed by general weakness, dizziness, and respiratory failure, leading to death. The mechanism of action is similar to that of saxitoxin and affects sodium channel permeability. 

Biochemical changes such as increased aminolaevulinate excretion and inhibition of amino-laevulinate dehydrase may be detected in urine and blood, respectively, at blood lead levels of 0.4 to 0.6 mg mL-1. Anemia is a late feature, however. Neurotoxicity may be detectable at blood lead levels of 0.8 to 1.0 mg mL-1. At blood lead levels greater than 1.2 mg mL-1, encephalopathy occurs. Peripheral nerve palsies are rare, and the foot and wrist drop, which were once characteristic of occupational lead poisoning, only occur after excessive exposure and are now rarely seen. Similarly, seizures and impaired consciousness may result from involvement of the CNS. Bone changes are usually seen in children and are detected as bands at the growing ends of the bones and a change in bone shape. 

This is a natural toxin, and poisoning results from eating contaminated shellfish. It causes gastrointestinal distress and disturbances and neurotoxicity. Domoic acid acts as an analogue of glutamate and as an excitotoxin excess excitation leading to neuronal cell death. 

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