Nicotine Exposure Along with Oral Contraceptive Treatment in Female Rats Exacerbates Post-cerebral Ischemic Hypoperfusion Potentially via Altered Histamine Metabolism

Author(s):  
Nathan d’Adesky ◽  
Francisca Diaz ◽  
Weizhao Zhao ◽  
Helen M. Bramlett ◽  
Miguel A. Perez-Pinzon ◽  
...  
2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e467-e468
Author(s):  
Lawrence Olatunji ◽  
Olugbenga Michael ◽  
Oluwaseun Adeyanju ◽  
Taofeek Usman ◽  
Emmanuel Areola ◽  
...  

Contraception ◽  
2005 ◽  
Vol 71 (5) ◽  
pp. 362-371 ◽  
Author(s):  
Makarios I. Eleftheriades ◽  
Irene V. Lambrinoudaki ◽  
George E. Christodoulakos ◽  
Odysseas V. Gregoriou ◽  
Emmanuel V. Economou ◽  
...  

1972 ◽  
Vol 50 (6) ◽  
pp. 539-544 ◽  
Author(s):  
J. LeBlanc ◽  
J. Côté ◽  
F. Doré ◽  
S. Rousseau

The basic nature of guanethidine and some of its effects suggested a possible action of this drug on histamine metabolism. A single intraperitoneal injection of guanethidine (10 mg/kg) in male rats was found to double the daily urinary excretion of free histamine; daily injection for three weeks caused a 10-fold increase. In male rats, guanethidine increased the number of mast cells in the peritoneal fluid and, in both peritoneal fluid and mesentery, caused a significant degranulation of these cells; this action was not observed in female rats. This finding may indicate that guanethidine blocks methylation of histamine by inhibiting imidazole methyl transferase since this enzyme is found in male but not in female rats. Bethanidine and reserpine had no effect on histamine excretion. Imidazole was found to be even more potent than guanethidine in causing an increase in urinary histamine. Guanethidine and imidazole neither potentiated nor mimicked the action of histamine on the isolated ileum.


2020 ◽  
Vol 209 ◽  
pp. 107927 ◽  
Author(s):  
Zachary R. Harmony ◽  
Erin M. Alderson ◽  
Israel Garcia-Carachure ◽  
Laurence D. Bituin ◽  
Cynthia A. Crawford

2009 ◽  
Vol 29 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Ben Ahmed Halima ◽  
Khlifi Sarra ◽  
Rtibi Kais ◽  
Elfazaa Salwa ◽  
Gharbi Najoua

Nicotine, a major toxic component of tobacco, has been identified as an important risk factor for infant and children diseases. It is concentrated in breast milk and is absorbed by the infant. The purpose of the present study was to investigate the effects of maternal nicotine exposure during lactation on breast-fed rats and at the pubertal age by measuring biomarkers of oxidative stress. Particularly, a new parameter, the thiol concentration was evaluated. Two groups of lactating Wistar rats were used. For the first group, female rats were given an intraperitoenal injection of nicotine or saline (2 mg/kg per day) during lactation. For the second group, we reproduced the same process described above and then the female and male pups were separately kept after weaning without any treatment until the puberty (at 45 days of age). In the liver and lung of the offspring, we examined the malondialdehyde (MDA) level, the thiol concentration, and the activities of two antioxidant enzymes: superoxyde dismutase (SOD) and catalase (CAT). In the plasma, alanine amino transferase (ALT) and aspartate amino transferase (AST) activities were measured. For rats aged 21 days, the treatment significantly reduced the thiol concentration, SOD, and CAT activities but increased MDA level, AST, and ALT activities. For rats aged 45 days, the males and females did not react the same way. In fact, the males were more affected. These results indicate that maternal nicotine exposure during the lactation period induces oxidative stress in the liver and lung of lactating offspring, which is maintained until the puberty, especially for the male rats.


2017 ◽  
Vol 69 (3) ◽  
pp. 512-519 ◽  
Author(s):  
Lawrence Aderemi Olatunji ◽  
Olugbenga Samuel Michael ◽  
Oluwaseun Aremu Adeyanju ◽  
Emmanuel Damilare Areola ◽  
Ayodele Olufemi Soladoye

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