Effects of Postnatal Exposure to Cigarette Smoke on Hypothalamic Catecholamine Nerve Terminal Systems and Neuroendocrine Function in Weanling and Adult Male Rats

1991 ◽  
pp. 331-337 ◽  
Author(s):  
K. Andersson ◽  
A. Jansson ◽  
B. Bjelke ◽  
P. Eneroth ◽  
K. Fuxe
Keyword(s):  
Cigarette Smoke ◽  
Nerve Terminal ◽  
Adult Male ◽  
Male Rats ◽  
Postnatal Exposure ◽  
Neuroendocrine Function

scholarly journals Effect of di(2-ethylhexyl) phthalate on the neuroendocrine regulation of reproduction in adult male rats and its relationship to anxiogenic behavior: Participation of GABAergic system

2018 ◽  
Vol 38 (1) ◽  
pp. 25-35 ◽  
Author(s):  
S Carbone ◽  
OJ Ponzo ◽  
N Gobetto ◽  
YA Samaniego ◽  
R Reynoso ◽  
...  
Keyword(s):  
Adult Male ◽  
Reproductive Tract ◽  
Consumer Products ◽  
Gabaergic System ◽  
Male Rats ◽  
Neuroendocrine Regulation ◽  
Gamma Aminobutyric Acid ◽  
Postnatal Exposure ◽  
Gaba Agonists ◽  
Ethylhexyl Phthalate

The endocrine disruptor di-(2-ethylhexyl) phthalate (DEHP) is used in a variety of consumer products made with polyvinyl chloride and also in the manufacture of medical devices. DEHP disrupts reproductive tract development in an antiandrogenic manner and also may induce neurobehavioral changes. The aim of this study was to investigate the effects of chronic postnatal exposure to DEHP (30 mg/kg body weight/day, orally from birth to day 60) on the neuroendocrine regulation of the gonadal axis and its impact on the anxiety-like behavior in adult male rats, as well as the probable participation of the GABAergic system in these effects. DEHP produced a significant increase in plasmatic luteinizing hormone and follicle stimulating hormone, as well as significant testosterone decrease, accompanied with a decrease in hypothalamic gamma-aminobutyric acid (GABA) concentration. On the other hand, DEHP increased the anxiety-like behavior in the elevated plus maze test, evidenced by a significant decrease in the percentages of time spent in the open arms and the frequency in the open arm entries and a significant increase in the percentage of time spent in closed arms. Neuroendocrine and behavioral effects were reversed by GABA agonists, muscimol (2 mg/kg i.p. ) and baclofen (10 mg/kg i.p.). In conclusion, chronic DEHP postnatal exposure induced a disruption in the neuroendocrine regulation of the testicular axis in young adult male rats, and this effect was correlated with an anxiety-like behavior. Since GABA agonists reversed these effects, the results suggest that GABA could participate in the modulation of reproductive and behavioral DEHP effects.

scholarly journals DREADD‐Induced Inhibition of the MnPO Affects Drinking Behavior and Neuroendocrine Function in Adult Male Rats

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Alexandria B. Marciante ◽  
George Farmer ◽  
Lei Wang ◽  
J. Thomas Cunningham
Keyword(s):  
Adult Male ◽  
Drinking Behavior ◽  
Male Rats ◽  
Neuroendocrine Function

Effects of cigarette smoke with different tar contents on hepatic and pulmonary xenobiotic metabolizing enzymes in rats

2002 ◽  
Vol 21 (1) ◽  
pp. 17-23 ◽  
Author(s):  
B C Eke ◽  
M İşcan
Keyword(s):  
Lipid Peroxidation ◽  
Cigarette Smoke ◽  
Adult Male ◽  
Ethacrynic Acid ◽  
Reduced Glutathione ◽  
Erod Activity ◽  
Male Rats ◽  
Glutathione S Transferase ◽  
Metabolizing Enzymes ◽  
Gst Activity

The effects of smoke from cigarettes with two different tar contents (32 mg/cigarette, high tar, and 15 mg/cigarette, low tar) on hepatic and pulmonary monooxygenase (MO) activities (aniline 4-hydroxylase [AH]; aminopyrine N-demethylase [AMND]; 7-ethoxyresorufin O-deethylase [EROD]; p-nitroanisole O-demethylase [p-NAOD]), lipid peroxidation (LP) and reduced glutathione (GSH) levels and glutathione S-transferase (GST) activities toward several substrates (1-chloro-2,4-dinitrobenzene [CDNB]; 1,2-dichloro-4-nitrobenzene [DCNB]; ethacrynic acid [EAA]; 1,2-epoxy-3-(p-nitrophenoxy)-propane [ENPP]) were determined in adult male rats. Adult male rats were exposed to smoke of high-or low-tar cigarettes five times a day, with 1-hour intervals, for 3 days in a chamber where smoke and fresh air lead alternatively and were killed 16 hours after the last treatment. Smoke of both high-and low-tar cigarettes (SHTCC and SLTCC) significantly increased hepatic and pulmonary EROD and p-NAOD activities compared to controls. However, the increase noted by SHTCC on pulmonary EROD activity was higher than that of SLTCC. Hepatic AMND and pulmonary AH activities were significantly increased only by SHTCC. LP level was significantly decreased and increased by SHTCC in liver and lung, respectively, whereas it remained unaltered by SLTCC. Only SHTCC significantly increased GSH level in liver. In the lungs, both SHTCC and SLTCC significantly increased GSH level to the same extent. Hepatic GST activity toward EAA was significantly increased by SHTCC but was significantly decreased by SLTCC. ENPP GST activity was significantly decreased by SHTCC and SLTCC in the livers. In the lungs, all the GST activities examined were significantly depressed by SHTCC whereas only GST activity toward DCNB was reduced significantly by SLTCC. These results reveal that the hepatic and pulmonary MOs and GSTs are differentially influenced by SHTCC and SLTCC in rats.

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