Nervous system toxicity behavioral changes

The precise mechanism of monomethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute toxicity of dimethylhydrazine exposure probably involves the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Additionally, renal and hepatic toxicity and hemolytic effects imply alternate mechanisms of toxicity. 

The precise mechanism of dimethylhydrazine toxicity is uncertain. In addition to the contact irritant effects, the acute effects of dimethylhydrazine exposure may involve the central nervous system as exemplified by tremors and convulsions (Shaffer and Wands 1973) and behavioral changes at sublethal doses (Streman et al. 1969). Back and Thomas (1963) noted that the deaths probably involve respiratory arrest and cardiovascular collapse. The central nervous system as a target is consistent with the delayed latency in response reported for dimethylhydrazine (Back and Thomas 1963). There is some evidence that 1,1-dimethylhydrazine may act as an inhibitor of glutamic acid decarboxylase, thereby adversely affecting the aminobutyric acid shunt, and could explain the latency of central-nervous-system effects (Back and Thomas 1963). Furthermore, vitamin B6 analogues that act as coenzymes in the aminobutyric acid shunt have been shown to be effective antagonists to 1,1-dimethylhydrazine toxicity (reviewed in Back and Thomas 1963). 

Neurotoxins The term refers to a specific target organ characterization of effect. Neurotoxins are chemicals which produce their primary toxic effects on the central nervous system. Signs and symptoms are narcosis, behavioral changes, and decrease in motor functions. Examples are mercury and carbon disulfide. 

Inhalation of high concentrations of ether produces central nervous system (CNS) changes, such as behavioral effects, excitation, depression, and unconsciousness. Male mice exposed by inhalation to 13 300-30 000 ppm of diethyl ether for 20 min had decreased excitability, reduced muscle tone, and reduced sensorimotor activity. Diethyl ether is a mild eye irritant. The reported toxic doses for mice include the following LC50 (inhalation), 31 000 ppm per 30 min LD50 (intraperitoneal), 2.4gkg and LD50 (intravenous) 996 mg kg... 

From the standpoint of screening and hazard identification, a notable point relating to the interpretation of data from FOB and motor activity studies is whether the effects observed in response to toxicant exposure represent a direct effect of the toxicant on the nervous system or are secondary to changes in other systems since such apical tests rely on the functional integrity of multiple systems. In some circumstances, the fact that the toxic effect is ultimately expressed in behavior may minimize the importance... 

CMs include AChE inhibition, particularly in the blood and brain behavioral and/or motor activity changes and developmental toxicity or developmental neurotoxicity. When EPA evaluates AChE data for risk assessment purposes, measurements of AChE from the target tis.sue — the central or peripheral nervous system — are preferred. Toxicology studies submitted to EPA for pesticide registration typically measure plasma, red blood cell (RBC), and brain cholinesterase (ChE) inhibition and most often do not measure peripheral tissues. In the absence of such data, EPA considers blood measures as surrogate.s of peripheral tissues,... 

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