Effect of acrylamide on biogenic amine levels, monoamine oxidase, and cathepsin D activity of rat brain

1981 ◽  
Vol 26 (1) ◽  
pp. 168-173 ◽  
Author(s):  
Rakesh Dixit ◽  
Rausan Husain ◽  
Hasan Mukhtar ◽  
Prahlad K. Seth
1979 ◽  
Vol 18 (10) ◽  
pp. 771-776 ◽  
Author(s):  
D.S. Robinson ◽  
I.C. Campbell ◽  
Margaret Walker ◽  
Nancy J. Statham ◽  
W. Lovenberg ◽  
...  

1992 ◽  
Vol 25 (3) ◽  
pp. 201-207 ◽  
Author(s):  
Stacey A. Jones-Humble ◽  
Ron M. Norton ◽  
Helen L. White ◽  
Barrett R. Cooper

1989 ◽  
Vol 23 (4) ◽  
pp. 454-456 ◽  
Author(s):  
A. Kenessey ◽  
M. Banay-Schwartz ◽  
T. de Guzman ◽  
A. Lajtha

2001 ◽  
Vol 88 (2) ◽  
pp. 75-80 ◽  
Author(s):  
Ling Dong Kong ◽  
Ren Xiang Tan ◽  
Anthony Yiu Ho Woo ◽  
Christopher Hon Ki Cheng2Note

1989 ◽  
Vol 16 (3) ◽  
pp. 281-286
Author(s):  
Olof Tottmar ◽  
Maria Söderbäck ◽  
Anders Aspberg

The development of monoamine oxidase (MAO) and aldehyde dehydrogenase (ALDH) in reaggregation cultures of fetal rat brain cells was compared with that of enzymatic markers for glial and neuronal cells. Only MAO-A was detected in the cultures during the first week, but, during the following three weeks, the activity of MAO-B increased more rapidly than that of MAO-A. The ratio MAO-A/MAO-B in four-week aggregates was close to that found in the adult rat brain. The activity of ALDH started to increase rapidly after 15 days, and the developmental pattern was intermediate to those of the glial and neuronal markers. The activity after four weeks was close to that found in the adult rat brain. Epidermal growth factor (EGF) caused a slight decrease in the activities of the low-Km ALDH (after four weeks) and the neuronal marker, choline acetyltransferase (after two weeks), whereas the other markers were not affected. By contrast, the activities of MAO-A and MAO-B were greatly increased during almost the entire culture period. It is suggested that this effect of EGF was the result of increased mitotic activity and/or biochemical differentiation of other cell types present in the cell aggregates, e.g. capillary endothelial cells.


1972 ◽  
Vol 127 (4) ◽  
pp. 705-713 ◽  
Author(s):  
Janet N. Ryan ◽  
J. Frederick Woessner

1. The earlier observation (Woessner, 1969) of oestradiol inhibition of collagen breakdown is confirmed and extended. Administration of 100μg of oestradiol-17β/day to parturient rats strongly inhibits the loss of collagen from the involuting uterus. Three experiments show that this effect is due to an inhibition of collagen degradation rather than to a stimulation of collagen synthesis. 2. Uterine collagen was labelled with hydroxy[14C]-proline by the administration of [14C]proline near the end of pregnancy. By 3 days post partum, control uteri lost 83% of their collagen and 90% of their hydroxy[14C]proline. Uteri from oestradiol-treated rats lost only 50% of both total and labelled hydroxyproline, with no decrease in the specific radioactivity of the hydroxyproline. 3. Incorporation of [14C]proline into uterine collagen hydroxyproline in vivo was not affected by oestradiol treatment. 4. Urinary excretion of hydroxyproline was increased in post-partum control rats and decreased in oestradiol-treated rats. 5. An enzyme capable of cleaving 4-phenylazobenzyloxycarbonyl-l-prolyl-l-leucylglycyl- l-prolyl-d-arginine (a substrate for clostridial collagenase) increased in activity in the post-partum uterus and was unaffected by oestradiol treatment. 6. Uterine homogenates digested uterine collagen extensively at pH3.2. This digestion was unaffected by the oestradiol treatment. 7. Lysosomal fractions prepared by density-gradient centrifugation of uterine homogenates contained coincident peaks of cathepsin D activity and peptide-bound hydroxyproline. The cathepsin D and hydroxyproline contents of this peak were unaffected by oestradiol treatment.


1985 ◽  
Vol 330 (2) ◽  
pp. 337-342 ◽  
Author(s):  
Thomas C. Rainbow ◽  
Bruce Parsons ◽  
Caroline M. Wieczorek ◽  
Scott Manaker

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