This hypothesis is based on the finding that testosterone has been shown to generate an oxidative stress in mammalian tissues (i.e. Chainy et al. 1997; Zhu et al. 1997). The allocation of these antioxidant pigments (i.e. carotenoids) to colourful traits (i.e. many red–yellow traits) would reduce the capacity to fight off ROS and might therefore further compromise the oxidative balance. Here, we tested the hypothesis that testosterone depresses resistance to oxidative stress in a species with a testosterone-dependent sexual signal, the zebra finch. (The funders had no role in study design, data collection and analysis, the decision to publish, or the preparation of the manuscript). IS and RR were involved in the study conception, data analyses and interpretation, discussing the results, and writing the paper. In conclusion, our data show that low testosterone reduces cardiac contractile function. Tissues were processed for both histological and gene and protein expression analysis and were archived for future analysis. The Tfm mouse was used as a model of testosterone deficiency and androgen receptor (AR) dysfunction as previously described 16–18. Androgen deprivation therapy for the treatment of prostate cancer in men, whilst reducing tumour growth, also increases the risk of coronary heart disease, diabetes and cardiovascular death, indicating that testosterone deficiency may promote atherosclerosis 8, 9. These exploratory data suggest that androgen deficiency may reduce the buffering capability for glucose uptake and utilisation in abdominal subcutaneous and muscle and fatty acids in abdominal subcutaneous. Moreover,the 19-oic androstenedione derivative contained an 18Oatom, which confirms the retention of the oxygen atoms in carboxylicacid functional groups during the workup conditions of the incubation(cf. Figure 1 control experiment and also withthe detection of 19-oic testosterone derivative by LC–MS).Hahn and Fishman had previously identified 2β-hydroxy-19-oxoandrostenedionein incubations with human placental microsomes.10,11 This product (the 19-oicacid of either androstenedione or testosterone) appears to be stableand was not converted to an estrogen (or 19-norandrogen) in P450 19A1incubations. In orderto simplify our results, we present the data obtained with the androstenedioneseries in this report; however, the results from the testosteroneseries are consistent with the androstendione work and are includedin the Supporting Information.
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