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Background: Depression and anxiety are frequent during pregnancy, and epidemiological studies demonstrate high rates of co-morbidity. Aims: To evaluate the association between the trait and state anxiety and depressive symptoms in women during the perinatal period. Method: A transversal study was conducted at the National Institute of Perinatology (INPer, Mexico City) from 2012 and 2015. Pregnant women diagnosed with Major Depressive Disorder (MDD) were included (N=128). Depressive and anxiety symptoms were evaluated using CES-D and STAI, respectively. Patients were sub-classified according to percentile 75 for Low and High Trait Anxiety (LTA, HTA) and Low and High State Anxiety (LSA, HSA); depressive symptoms were compared between pregnant women and women in the postpartum, by state and trait levels. Results: CES-D scores differed according to state and trait anxiety levels: while we observed that depressive scores (CES-D) were higher in HTA patients compared to LTA prenatally (35.9±9,5 vs 21.2±10,8 respectively; p=0.001), this finding was not observed in the postpartum period. In the case of state anxiety depressive scores were elevated among HSA versus LSA groups before delivery (33.0±11.3 vs 14.0±6.7 respectively; p=0.008) and after partum (35.1±8.06 vs 10.0±6.0; p=0.005). Conclusions: Patients showed higher scores of depressive symptoms when high trait or state anxiety comorbidity is present during the perinatal period. In the postpartum period, even low trait anxiety scores were associated with high depressive scores.

Background: Depression and anxiety are frequent during pregnancy, and epidemiological studies demonstrate high rates of co-morbidity. Aims: To evaluate the association between the trait and state anxiety and depressive symptoms in women during the perinatal period. Method: A transversal study was conducted at the National Institute of Perinatology (INPer, Mexico City) from 2012 and 2015. Pregnant women diagnosed with Major Depressive Disorder (MDD) were included (N=128). Depressive and anxiety symptoms were evaluated using CES-D and STAI, respectively. Patients were sub-classified according to percentile 75 for Low and High Trait Anxiety (LTA, HTA) and Low and High State Anxiety (LSA, HSA); depressive symptoms were compared between pregnant women and women in the postpartum, by state and trait levels. Results: CES-D scores differed according to state and trait anxiety levels: while we observed that depressive scores (CES-D) were higher in HTA patients compared to LTA prenatally (35.9±9,5 vs 21.2±10,8 respectively; p=0.001), this finding was not observed in the postpartum period. In the case of state anxiety depressive scores were elevated among HSA versus LSA groups before delivery (33.0±11.3 vs 14.0±6.7 respectively; p=0.008) and after partum (35.1±8.06 vs 10.0±6.0; p=0.005). Conclusions: Patients showed higher scores of depressive symptoms when high trait or state anxiety comorbidity is present during the perinatal period. In the postpartum period, even low trait anxiety scores were associated with high depressive scores.

Acetaldehyde (Ac), the main metabolite of ethanol oxidation, is a very reactive compound involved in alcohol-induced liver damage. In the present work, we studied the effect of Ac in mitochondria functionality. Mitochondria from Wistar rats were isolated and treated with Ac. Ac decreased respiratory control by 50% which was associated with a decrease in adenosine triphosphate content (28.5%). These results suggested that Ac could be inducing changes in cell redox status. We determined protein oxidation, superoxide dismutase (SOD) activity, and glutathione ratio, indicating that Ac induced an enhanced oxidation of proteins and a decrease in SOD activity (90%) and glutathione/oxidized GSH ratio (36%). The data suggested that Ac-induced oxidative stress mediated by mitochondria dysfunction can lead to cell sensitization and to a second oxidative challenge. We pretreated hepatocytes with Ac followed by treatment with antimycin A, and this experiment revealed a noticeable decrease in cell viability, determined by neutral red assay, in comparison with cells treated with Ac alone. Our data demonstrate that Ac impairs mitochondria functionality generating oxidative stress that sensitizes cells to a second damaging signal contributing to the development of alcoholic liver disease.

Affiliation 1 is incomplete. It should read: 1. Department of Experimental Medicine, School of Medicine, Universidad Nacional Autonoma de Mexico (UNAM), Hospital General de Mexico, Mexico City, Mexico.