toxicity

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toxicity

[täk′sis·əd·ē]
(pharmacology)
The quality of being toxic.
The kind and amount of poison or toxin produced by a microorganism, or possessed by a chemical substance not of biological origin.
References in periodicals archive ?
The drug caused decreased fetal body weights, increased fetal structural variations, and maternal toxicity when the drug was given to pregnant rabbits throughout organogenesis.
The reduction in body weight gain of rats from groups exposed to 300 and 1000 mg [kg.sup.-1] bw [day.sup.-1] and the absent significant difference in number of live fetuses and mean fetal weight indicate that in Wistar rats the LOEL was 300 mg [kg.sup.-1] bw [day.sup.-1] and NOEL was 150 mg [kg.sup.-1] bw [day.sup.-1] (maternal toxicity).
This study did not demonstrate maternal toxicity and anti-implantation effect; however, there was reduction of fetal body mass, which might indicate possible embryofoetotoxicity.
Rabbits 200 ppm Maternal toxicity, embryo toxicity 100 ppm NOEL
Doses that resulted in exposures that were less than the human exposure caused maternal toxicity, abortions, and embryo-fetal death.
In support of this interpretation, higher doses of parathion administered to pregnant rats throughout gestation do affect ChAT but only when the dose is sufficiently high to elicit clear signs of maternal toxicity and down-regulation of mAChR binding (Gupta et al.
Use of injectable anesthetics tor dental procedures also is common in pregnancy Maternal toxicity involving the central nervous and cardiovascular systems may result from inadvertent intravenous administration or excessive doses.
Heptachlor and dieldrin administered to pregnant rats, although causing some maternal toxicity, resulted in increased activity of striatal DAT in offspring exposed during gestational, perinatal, and adolescent periods (Purkerson-Parker et al.
Conventional developmental and reproductive toxicology assays in mice, rats, and rabbits consistently fail to find adverse effects of TCE on fertility or embryonic development aside from embryo- or fetotoxicity associated with maternal toxicity [Cosby and Dukelow 1992; Dorfmueller et al.
The highest DEBT dose--a huge dose, far higher than the normal human dose--was associated with maternal toxicity (reduced body weight and food consumption) and lower birth weights in the offspring; there was no evidence of fetal toxicity or malformations, regardless of the dose used.
In those studies, exposure to PFOS during pregnancy led to significant physiologic alterations that indicate maternal toxicity. In addition, these results indicate that in utero exposure to PFOS severely compromises postnatal survival of neonatal rats and mice and causes delays in growth and development accompanied by hypothyroxinemia in the surviving rat pups.

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