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Nigel P. Moore Shakil A. Saghir Amy J. Clark Steven C. Hansen Edward W. Carney Valerie A. Marshall Reza Rasoulpour Michael J. Bartels 《Birth defects research. Part B, Developmental and reproductive toxicology》2012,95(2):107-115
N‐(2‐aminoethyl)ethanolamine (AEEA) caused aneurysms of the great vessels in rats exposed in utero and during the first days post partum, exacerbated by postnatal treatment of the lactating dams (Moore et al., 2012. Birth Defects Res B Dev Reprod Toxicol [95:116‐122]). The purpose of this work was to examine the systemic availability of AEEA during gestation and early lactation. The absorption of AEEA was determined following oral administration to nonpregnant and pregnant female Wistar rats. A single dose administered by gavage (0.5 or 50 mg/kg) on gestation day 18 was rapidly and extensively (>90%) absorbed from the gastrointestinal tract (absorption t1/2 = 0.1–0.2 hr). Elimination from the plasma followed a biphasic pattern, with a rapid elimination phase (t1/2 α = 1.6–1.8 hr) followed by a slower phase (t1/2 β = 16.7–17.3 hr). Following repeated gavage administration during gestation day 17 to 19, 14C‐AEEA–derived radioactivity readily partitioned into the fetus and was evenly distributed therein, but cleared approximately twofold slower from the fetal blood and tissues than the maternal blood and chorioallantoic placenta. When administered to lactating dams during lactation days 1 to 12, 14C‐AEEA–derived radioactivity preferentially partitioned into the milk reaching levels that were between 1.6‐ and 2.5‐fold higher than the maternal blood. Although the concentration of AEEA equivalents in the maternal blood remained quite consistent, the concentration in the milk fell by almost 40% between lactation days 4 and 12, probably reflecting an increase in milk production over this same period. We confirm exposure of the offspring to AEEA both in utero and during lactation, but that AEEA does not appear to specifically concentrate in the great vessels. 相似文献
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Gisela Mäck 《Planta》1998,205(1):113-120
A cytosolic and a plastidic isoenzyme of glutamine synthetase (GS; EC 6.3.1.2) were separated from hairy roots of Beta vulgaris L. var. lutea. The predominant activity was that of cytosolic GS 1; the relative proportion of plastidic GS 2 activity changed, however,
depending on the growth conditions. Maximum activity of both isoenzymes was measured after growth with NO−
3 as the major N-source. Growth with NH+
4 as the sole N-source or growth in constant darkness resulted in a significant decrease in GS 1 activity, whereas GS 2 activity
was much less effected and thus contributed as much as 25% of total root GS activity. The isoenzymes GS 1 and GS 2 were active
both in the octameric and tetrameric states. Both oligomers of GS 2 and octameric GS 1 were active under all growth conditions
applied whereas tetrameric GS 1 was not active when the roots were grown under light-dark changes with NO−
3 as the major N-source. The molecular masses of the subunits were identical for both isoenzymes. Glutamine synthetase 1 was
composed of up␣to four different 38-kDa subunits and two different 41-kDa subunits; GS 2 was assembled from one type of 38-kDa
subunit and one type of 41-kDa subunit. The GS␣2 subunits were most probably identical to two of the GS␣1 subunits. The subunit
composition of GS 1, but not of GS 2, changed depending on the growth conditions of the roots. Changes in GS 1 subunit composition
were correlated with changes in GS 1 activity. The different growth conditions induced the specific assembly of different
GS 1 isoenzymes which could, however, not be separated by anion-exchange chromatography but became evident only after two-dimensional
sodium dodecyl sulfate-polyacrylamide gel electrophoresis.
Received: 30 May 1997 / Accepted: 28 August 1997 相似文献
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C. S. Casley L. Canevari J. M. Land † J. B. Clark M. A. Sharpe 《Journal of neurochemistry》2002,80(1):91-100
Disrupted energy metabolism, in particular reduced activity of cytochrome oxidase (EC 1.9.3.1), alpha-ketoglutarate dehydrogenase (EC 1.2.4.2) and pyruvate dehydrogenase (EC 1.2.4.1) have been reported in post-mortem Alzheimer's disease brain. beta-Amyloid is strongly implicated in Alzheimer's pathology and can be formed intracellularly in neurones. We have investigated the possibility that beta-amyloid itself disrupts mitochondrial function. Isolated rat brain mitochondria have been incubated with the beta-amyloid alone or together with nitric oxide, which is known to be elevated in Alzheimer's brain. Mitochondrial respiration, electron transport chain complex activities, alpha-ketoglutarate dehydrogenase activity and pyruvate dehydrogenase activity have been measured. Beta-amyloid caused a significant reduction in state 3 and state 4 mitochondrial respiration that was further diminished by the addition of nitric oxide. Cytochrome oxidase, alpha-ketoglutarate dehydrogenase and pyruvate dehydrogenase activities were inhibited by beta-amyloid. The K(m) of cytochrome oxidase for reduced cytochrome c was raised by beta-amyloid. We conclude that beta-amyloid can directly disrupt mitochondrial function, inhibits key enzymes and may contribute to the deficiency of energy metabolism seen in Alzheimer's disease. 相似文献
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