Toxicity neurotoxic effects

Golgi a-l)-mannosidase II lysosomal mannosidase glycoprotein A-linked oligosaccharide processing [toxic, neurotoxic effects mimic hereditary lysosomal storage disease mannosidosis] (3-D-Glucuronidase cx-1-iduronidase Glucosidase... 

One noteworthy neurotoxic response was demonstrated in laboratory pyrolysis studies using various types of phosphoms flame retardants in rigid urethane foam, but the response was traced to a highly specific interaction of trimethylolpropane polyols, producing a toxic bicycHc trimethylolpropane phosphate [1005-93-2] (152). Formulations with the same phosphoms flame retardants but other polyols avoided this neurotoxic effect completely. 

Antituberculin Agents. Rifampin [13292-46-17, a semisynthetic derivative of rifamycin SV, is a most valuable dmg for treatment of tuberculosis, an infection caused by mycobacteria, leprosy, and an expanding range of other infections (23). Cycloserine [64-41-7] has been used to a limited extent for treatment of tuberculosis as a reserve dmg. Although cycloserine inhibits bacteria by interfering with their cell wall biosynthesis, it has toxic side effects in humans in the form of neurotoxicity. Capreomycin [11003-38-6] and to a much lesser extent viomycin [32988-50-4] both of which are peptides, have also been used for treatment of this disease. 

In summary, neurotoxic effects of endosulfan are usually apparent only after acute ingestion of relatively high doses. Cumulative neurotoxicity does not appear to be significant. If the animal survives the acute toxic effects, then no long-term neurotoxic effects are evident from behavioral, gross, and microscopic observations. However, some impairment may occur that can be detected only by specialized neurobehavioral testing. 

Human toxicity Acute effects Carcinogenicity Genotoxicity/mutagenicity Developmental Teratogenicity/mutagenicity Neurotoxicity Endocrine disruption... 

The priority effects are carcinogenicity, mutagenicity, reproductive or developmental toxicity, endocrine disruption and neurotoxicity. Human toxicity is broader than priority effects, including acute toxicity, systemic toxicity (organ effects), immune system effects and skin/eye/respiratory damageaswellasthepriority effects. And toxicity as T includes both human toxicity and ecotoxicity. 

Brain is a key tissue to analyze for mercury concentration because it is the site of MeHg toxicity. The neurotoxic effects of MeHg in adrrlt mammals inclnde ataxia, difficulty in locomotion neurasthenia, a generalized weakness impairment of hearing... 

This chapter will review some recently completed studies on the long-term effects of MDMA in nonhuman primates. The goals of these studies were to (1) determine if the neurotoxic effects of MDMA, which have been well documented in the rodent (see below), generalize to the primate (2) compare the relative sensitivity of primates and rodents to the neurotoxic effects of MDMA (3) ascertain if the toxic effects of MDMA in the monkey are restricted to nerve fibers (as they are in the rat), or if they involve cell bodies as well (4) evaluate how closely toxic doses of MDMA in the monkey approximate those used by humans and (5) examine whether 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF) can be used to detect MDMA-induced serotonergic damage in the CNS of primates. Before presenting the results of these studies, previous results in the... 

The results of the studies reviewed here show that the neurotoxic effects of MDMA generalize to the primate. Further, they indicate that monkeys are considerably more sensitive than rats to the serotonin-depleting effects of MDMA, and that the dose-response curve of MDMA in the monkey is much steeper than in the rat. Perhaps as a consequence of this, the toxic effects of MDMA in the monkey involve serotonergic nerve fibers as well as cell bodies, whereas in the rat, only nerve fibers are affected. The present studies also show that the toxic dose of MDMA in the monkey... 

The possibility that an aetive metabolite is involved in the neurotoxic effects of amphetamine analogs reeeives limited discussion in this chapter and has been considered previously, espeeially with />-chloroamphetamine (Miller et al. 1986.) Partly beeause the ehemieal structures of these amphetamines do not suggest ways in whieh they would be toxic to neurons, the... 

RESPONSE We do not understand all there is to know about the mechanisms of MPTP neurotoxicity, but it seems to involve MPP+, which is potentially cytotoxic to all cells but that attains toxic concentrations after MPTP administration only in cells that concentrate MPP+. Dopamine apparently is not involved in the neurotoxic effects of MPTP. I am attracted to the idea that dopamine itself may be involved in the etiology of Parkinson s disease, that dopamine neurons may be at risk because of the nature of their neurotransmitter. 

No NOAELs or LOAELs were identified for toxic effects in humans after inhalation exposure to organophosphate ester hydraulic fluids. Reliable NOAELs and LOAELs for acute inhalation exposure are restricted to 4-hour NOAELs for systemic effects in rats exposed to Fyrquel 220 or Durad MP280 and 4-hour LOAELs for mild lethargy in rats exposed to Durad MP280 and Fyrquel 220 (Gaworski et al. 1986). The study identifying these NOAEL and LOAEL values did not measure cholinesterase inhibition, did not allow sufficient follow-up time for the development of delayed neurotoxic effects, and used a... 

Neurotoxicity. There is a very large database on the neurotoxic effects of lead. The most severe neurobehavioral effect of lead toxicity in adults is lead encephalopathy (Kehoe 1961a Kumar et al. 1987 Smith et al. 1978). Early symptoms, which may develop within weeks of initial exposure, include dullness, irritability, poor attention span, headache, muscular tremor, loss of memory, and hallucinations. These symptoms worsen, sometimes abruptly, to delirium, convulsions, paralysis, coma, and death. 

Fig. 6 Biomonitoring of pollution in the Ebro Delta with Daphnia magna and Corbicula fluminea. (a) Map of sampling sites. Site 1 is out of the figure limits, close to Amposta (see Fig. 1). (b) Assays for neurotoxic activity (ChE and CbE) and D. magna feeding). Note the different pattern for the microcrustacean (sensitive to insecticides), which show a maximal toxic (inhibitory) effect in May and June, and the mollusk (relatively resistant), (c) Oxidative stress markers. These markers showed a similar response for both species with maximal effects (activation) in May (month 5) and August (month 8). Data from [43] and [44], Dm and Cf identify markers from D. magna and C. fluminea, respectively...

The results of the investigation of 58 adult persons who live on industry territory of North Crimea and 60 male teenagers at age 15 years and 84 children (2-14 years) in the Simferopol city showed that the children are more sensitive to the relatively low level of heavy metal concentrations than the adult (Evstafyeva et al., 2002). It is known that many toxic metals have neurotoxic effects (Arezzo et al., 1985). It was also shown that the effects of central and autonomous nervous systems of different... 

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