The haploinsufficiency of the tyrosine hydroxylase (TH-HZ) gene in female mice has been recently described as a model of premature aging. This catecholamine deficiency disrupts the function of the nervous… Click to show full abstract
The haploinsufficiency of the tyrosine hydroxylase (TH-HZ) gene in female mice has been recently described as a model of premature aging. This catecholamine deficiency disrupts the function of the nervous and immune systems, provoking an early establishment of an oxidative stress. In addition, these systems could be affected by the social environment (SE), in which an animal lives. Thus, the aim of the present work was to analyze the oxidative status of different organs in TH-HZ mice, as well to determine if the SE could modulate it. Female ICR-CD1 TH-HZ and wild-type (WT) mice were housed in six groups after weaning: WT, WT>50% (the proportion of WT mice was higher than 50% in relation to TH-HZ), WT could be reversed by SE. By contrast, SE seems to be prejudicial for WT mice. In conclusion, the catecholamine deficiency produces a worsened redox state that is ameliorated by SE.
               
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