Central Nervous System damage

Toews AD, Barrett C, Morell P (1998) Monocyte chemoattractant protein 1 is responsible for macrophage recruitment following injury to sciatic nerve. J Neurosci Res 53 260-267 Toggas SM, MasUah E, Rockenstein EM, Rail GF, Abraham CR, Mucke L (1994) Central nervous system damage produced by expression of the HIV-1 coat protein gpl20 in transgenic mice. Nature 367 188-189... 

Prevent central nervous system damage, including stroke... 

Toxicology. Acute exposure to high concentrations of mercury vapor causes severe respiratory damage, whereas chronic exposure to lower levels is primarily associated with central nervous system damage and renal effects. 

Yarbrough BE, et al Severe central nervous system damage and profound acidosis in... 

Toxicology. 2,4-Pentanedione is moderately irritating to the skin and eyes repeated exposure to high concentrations causes dyspnea, central nervous system damage, and death. 

Growth Animals deprived of vitamin A initially lose their appetites, possibly because of keratinization of the taste buds. Bone gcwlh is slow and fails to keep pace with growth of the nervous system, leading to central nervous system damage. 

Toluene 110 Yes Yes nausea headache mild anemia central nervous system damage (less toxic than benzene)... 

Mercury (Hg) is a toxic metal—it is one of the so-called heavy metals. Hg is a neurotoxin that causes damage to the central nervous system (CNS), which consists of the brain and associated parts. Hg is active at about 50pg/100mL of blood (500 ppb). Central nervous system damage manifests itself as quarrelsome behavior, headaches, depression, and muscle tremors. The classic example of mercury poisoning is the mad hatter, caused by mercury exposure during the felt-making process. 

Thiamin-Responsive Pyruvate Dehydrogenase Deficiency Genetic deficiency of pyruvate dehydrogenase Ela (which is on the X chromosome) leads to potentially fatal lactic acidosis, with psychomotor retardation, central nervous system damage, atrophy of muscle fibers and ataxia, and developmental delay. At least some cases respond to the administration of high doses (20 to 3,000 mg per day) of thiamin. In those cases where the enzyme has been studied, there is a considerable increase in the of the enzyme for thiamin diphosphate. Female carriers of this X-linked disease are affected to a variable extent, depending on the X-chromosome inactivation pattern in different tissues (Robinson et al., 1996). 

Burk RF, Christensen JM, Maguire MJ, Austin LM, WhetseU WO Jr, May JM, HUl KE, Ebner FF (2006) A Combined deficiency of vitamins E and C causes severe central nervous system damage in guinea pigs. J Nutr 136(6) 1576-1581... 

SAFETY PROFILE Poison by ingestion, subcutaneous, intravenous, and intraperitoneal routes. Experimental reproductive effects. Chronic exposure causes central nervous system damage and blood-pressure effects. When heated to decomposition it emits toxic NOx. See other amphetamine entries. 

Williams KC, Hickey WF (2002) Central nervous system damage, monocytes and macrophages, and neurological disorders in AIDS. Annu Rev Neurosci 25 537-562. 

Ocular malformations, including aplasia of the macula, choroidal colobomata, microphthalmos, and extraocular muscle paresis have been attributed to thalidomide taken in early pregnancy (135). Ocular defects have been reported in four of 21 thalidomide children examined in Canada there was strabismus in two cases, congenital blepharoptosis in one, and ocular muscle palsies associated with other central nervous system damage in one (136). 

Observe normal precautions appropriate to the circumstances and quantity of material handled. Phenylmercuric acetate may be irritant to the skin, eyes, and mucous membranes. Eye protection, gloves, and a respirator are recommended. Chronic exposure via any route can lead to central nervous system damage. In the UK, the occupational exposure limit for mercury-containing compounds, calculated as mercury, is 0.01 mg/m long-term (8-hour TWA) and 0.03 mg/m shortterm. ... 

Studies that have investigated inhalation of mold and mold products found that inhalation produces more potent effects than ingestion. These effects are as potent as intravenous administration. Mycotoxins upon inhalation may produce immunosuppression, carcinogenesis, cytotoxicity, neurotoxicity (including acute or chronic central nervous system damage), mucous membrane irritation, skin rash, nausea, acute or chronic liver damage, and endocrine effects. These effects may be independent of infection or stimulation of antibodies (in contrast to the Mycobacterium mycotoxins). 

TNT stains the skin orange and yellow. It can cause dermatitis, irritation of eyes, nose, throat, and skin. High exposures may cause weakness, anemia, headaches, liver, or central nervous system damage. 

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