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Fetal brain

Data from a single study in dogs suggest that hepatic first-pass metabolism may limit systemic availability of the parent compound following oral exposure (Braeckman et al. 1983). Placental transfer of methyl parathion was demonstrated in pregnant rats 1-3 days before parturition. Thirty minutes after administration, both methyl parathion and methyl paraoxon were found in fetal brain, liver, and muscle methyl parathion, but not methyl paraoxon, was detected in placenta and maternal liver (Ackermann and Engst 1970). Methyl parathion binds reversibly to serum albumin, but is readily distributed to the tissues (Braeckman et al. 1980, 1983). [Pg.100]

Logdberg B, Berlin M, Schutz A. 1987. Effects of lead exposure on pregnancy outcome and the fetal brain of squirrel monkeys. Scand J Work Environ Health 13 135-145. [Pg.545]

Phosphorylation is developmentally regulated, such that in fetal brain, tau is more heavily phosphorylated than in adult brain. An increase in tau phosphorylation reminiscent of that present during development was... [Pg.752]

Okonmah AD, Brown JW, Blyden GT, Soliman KF. (1988). Prenatal effects of acute harmaline exposure on fetal brain biogenic amine metabolism. Pharmacology. 37(3) 203-8. [Pg.547]

Apoptosis is induced by chohne deficiency in fetal brain and in PC 12 cells. Brain Res. [Pg.224]

CYP21 mRNA detected in fetal brain by RT-RT-PCR (Pezzi et al., 2003). [Pg.51]

Protein identified by IHC in the ventral pallidum, cerebral cortex, the amygdaloid area, the nucleus of the diagonal band, others of rat brain (Shinoda et al., 1989). Less activity in human fetal brain than other tissues assayed by pH] release from 1-androstenedione into water (Doody and Carr, 1989). [Pg.51]

Aromatase immunoreactivity in rat, human glioblastoma (Yague et al., 2004). Human fetal brain and intestine had more CYP19 mRNA than other tissues (Price et al., 1992). [Pg.51]

Hypothyroid women frequently have anovulatory cycles and are therefore relatively infertile until restoration of the euthyroid state. This has led to the widespread use of thyroid hormone for infertility, although there is no evidence for its usefulness in infertile euthyroid patients. In a pregnant hypothyroid patient receiving thyroxine, it is extremely important that the daily dose of thyroxine be adequate because early development of the fetal brain depends on maternal thyroxine. In many hypothyroid patients, an increase in the thyroxine dose (about 30-50%) is required to normalize the serum TSH level during pregnancy. Because of the elevated maternal TBG levels and, therefore, elevated total T4 levels, adequate maternal thyroxine dosages warrant maintenance of TSH between 0.5 and 3.0 mll/L and the total T4 at or above the upper range of normal. [Pg.867]

TABLE 3.2 Fatty acid composition of the fetal brain lipid in pregnancy rat administrated phospholipid samples by probe (%)... [Pg.34]

Engraftment of sorted/expanded human central nervous system stem cells from fetal brain. Tamaki, S., Eckert, K., He, D., Sutton, R., Doshe, M., Jain, G., Tushinski, R., Reitsma, M., Harris, B., Tsukamoto, A., Gage, F., Weissman, I., Uchida, N. (2002). J Neurosci Res, 69 (6) 976-986. [Pg.57]

Zoeller RT, Crofton RM. 2000. Thyroid hormone action in fetal brain development and potential for distribution by environmental chemicals. Neurotoxicology 21(6) 935-946. [Pg.460]


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