Browsing by Subject "Acetaminophen"

Now showing 1 - 3 of 3
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    Is maternal use of Paracetamol during pregnancy associated with anogenital distance in male newborns? The results from the NELA Birth Cohort
    (MDPI, 2021-06-11) Navarro Lafuente, Fuensanta; Arense Gonzalo, Julián Jesús; Adoamnei, Evdochia; Prieto Sánchez, María Teresa; Sánchez Ferrer, María Luisa; García-Marcos Álvarez, Luis Vicente; Morales Bartolomé, Eva; Mendiola Olivares, Jaime; Torres Cantero, Alberto Manuel; Ciencias Sociosanitarias
    Paracetamol is the one of the most commonly used medications during pregnancy. However, its potential antiandrogenic effect has been suggested. The objective of this study was to evaluate associations between maternal paracetamol use during pregnancy and anogenital distance (AGD) in male newborns from a Spanish birth cohort. The study included two hundred and seventy-seven mother-male child pairs with self-reported paracetamol use and frequency during each trimester of pregnancy. AGD measurements were taken employing standardized methods. The associations between maternal paracetamol use and AGD measures were evaluated using linear regression models, adjusting for potential confounders and covariates. Overall, 61.7% of pregnant women consumed paracetamol at any time of pregnancy with an average of 9.43 (SD = 15.33) days throughout pregnancy. No associations between the maternal use of paracetamol or its frequency and AGD measures among different trimesters or during the whole pregnancy were found in the adjusted final models. A non-differential misclassification error may have occurred—the recall of paracetamol intake independent of AGD measurements—introducing bias towards the null hypothesis. Nevertheless, the current evidence suggests that paracetamol might have a potential antiandrogenic effect especially in the early stages of fetal development. Thus, it would be highly recommendable to pursue further studies to elucidate the potential effects of paracetamol in human perinatal health and its use among pregnant women.
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    The effect of glucagon and cyclic adenosine monophosphate on acute liver damage induced by acetaminophen
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Kelava, Tomislav; Ćavar, Ivan; Vukojevic, Katarina; Saraga-Babić, Mirna; Čulo, Filip
    Recent investigations suggest that glucagon might have a potentially important hepatoprotective activity. We investigated the effect of glucagon in a model of acetaminophen-induced liver injury. CBA male mice were injected intraperitoneally with a lethal (300 mg/kg) or sublethal (150 mg/kg) dose of acetaminophen. The liver injury was assessed by observing the survival of mice, by liver histology and by measuring the concentration of alanine-aminotransferase (ALT). Inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF-κB) protein expressions were determined immunohistochemically. Hepatic levels of reduced glutathione (GSH) and cyclic adenosine monophosphate (cAMP) were also measured. Results show that glucagon, dose and time dependently, protects against acetaminophen-induced hepatotoxicity. This protection was achieved with a dose of 0.5 mg/kg of glucagon given intraperitoneally 15 min before or 1 h after acetaminophen. Treatment of animals with acetaminophen elevated ALT and nitrite/nitrate concentration in the plasma, enhanced iNOS and NF-κB expression and reduced GSH and cAMP concentration in the liver. Animals treated with glucagon had higher hepatic cAMP level, lower ALT and nitrite/nitrate concentration in plasma and lower expression of iNOS in liver cells than animals in control group, whereas there was no difference in the expression of NF-κB. Glucagon did not prevent the loss of GSH content caused by acetaminophen. Our investigation indicates that glucagon has a moderately protective effect against acetaminophen-induced liver injury, which is, at least partially, mediated through the downregulation of iNOS and through the increase in hepatic cAMP content, but it is not mediated through the modulation of NF-κB activity.
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    The role of prostaglandin E2 in acute acetaminophen hepatotoxicity in mice
    (Murcia : F. Hernández, 2010) Ćavar, Ivan; Kelava, Tomislav; Vukojevic, Katarina; Saraga-Babić, Mirna; Čulo, Filip
    Prostaglandin E2 (PGE2), which is synthesized by many cell types, has a cytoprotective effect in the gastrointestinal tract and in several other tissues and cells. On the other hand, overdose or chronic use of a high dose of acetaminophen (Paracetamol, APAP) is a major cause of acute liver failure in the western world. These observations prompted us to investigate whether PGE2 plays a role in host defence to toxic effect of APAP. (CBAT6T6xC57Bl/6)F1 hybrid mice of both sexes were intoxicated with a single lethal or high sublethal dose of APAP, which was administered to animals by oral gavage. Stabile analogue of PGE2, 16,16-dimethyl PGE2 (dmPGE2), or inhibitor of its production, CAY10526, were given intraperitoneally (i.p.) 30 minutes before or 2 hours after APAP administration. The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring concentration of alanine-aminotransferase (ALT) in plasma 20-22 hours after APAP administration and by liver histology. The results have shown that PGE2 exhibits a strong hepatoprotective effect when it is given to mice either before or after APAP, while CAY10526 demonstrated mainly the opposite effect. Immunohistochemical or immunofluorescent examinations in the liver tissue generally support these findings, suggesting that PGE2 inhibited APAP-induced activation of nuclear factor kappa B (NF-κB). Similarly, PGE2 down regulated the activity of inducible nitric oxide synthase (iNOS), which was up regulated by APAP. Thus, by these and perhaps by other mechanisms, PGE2 contributes to the defence of the organism to noxious effects of xenobiotics on the liver.