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Oxidative stress is the result of an imbalance between the production of reactive oxygen species (ROS) and antioxidant defences (Finkel & Holbrook 2000). Among them, the trade-off between immune functioning and testosterone-dependent sexual signals might reflect the differential allocation of energy/resources to the two functions, instead of a direct immunosuppressive effect of testosterone (Wedekind & Folstad 1994; Casto et al. 2001; Wikelski & Ricklefs 2001). The immunocompetence handicap hypothesis is based on the assumption that high circulating levels of testosterone, necessary for the full development of the signal, can also entail a cost due to the higher risk of mortality derived from the immunosuppressive properties of this steroid. We also found that cell-mediated immune response was depressed in testosterone-treated birds, supporting the immunocompetence handicap hypothesis. In agreement with the prediction, we found that red blood cell resistance to a free radical attack was the highest in males implanted with flutamide and the lowest in males implanted with testosterone. However, the cost of testosterone-based signalling is not limited to immunosuppression and might involve other physiological functions such as the antioxidant machinery.
Our data showed that orchidectomy significantly decreased myocardial contractility after twelve weeks of hormone deprivation. Individual mitochondrial subpopulations were isolated from SHAM, OQT and OQT+T and polarographic measurements were performed to index oxygen consumption under state 3 respiration conditions. The isometric force (g/g) in the left ventricular papillary muscles at baseline (A), and at different extracellular CaCl2 (0.62, 1.25, 2.5 and 3.75 mM) concentrations (B). Apocynin prevented the reduction of myocardial contractility (A, B) and mitochondrial function (C–F).
In addition to the above, Table 1 lists a wide variety of different industrial and environmental toxicants that are all capable of compromising male fertility by inducing a state of oxidative stress in the testes. In this situation, the oxidative stress induced in the testes by acute iron overload must have so damaged the DNA in the spermatozoa that the resulting embryos were non-viable. Table 1 also highlights a number of metals that are known to induce oxidative stress in the testes and compromise male infertility. The relevance of this model to the oxidative stress detected in cases of varicocele is clearly suggested by the effects of varicocelectomy. The latter then induce high levels of peroxidative damage via mechanisms that are enhanced by the local release of transition metals. Significantly, the level of peroxidative damage observed in testicular tissue increases following detorsion, indicating the induction of reperfusion injury.54 The biochemical basis for reperfusion injury is thought to involve a key metabolic enzyme, xanthine dehydrogenase, which becomes converted to a xanthine oxidase during ischaemia, due to oxidation of essential -SH groups and/or a limited proteolytic clip.
As shown in Figure 1D, Serca2a protein expression was significantly decreased in the OQT group and this decrease was prevented by testosterone replacement. To identify carbonyl groups that are introduced into the amino acid side chains after oxidative modification of proteins, 2D-oxyblot analysis was performed (29). In conclusion, our findings demonstrate that testosterone deficiency leads to reduced myocardial contractility and impaired cardiac interfibrillar mitochondrial function. Orchidectomy increased total left ventricular mitochondrial protein in the SSM, but not in IFM. Considering the intimate connection between oxidative metabolism and myocardial contractility, we determined the effects of testosterone deficiency on the two spatially distinct subpopulations of cardiac mitochondria, subsarcolemmal (SSM) and interfibrillar (IFM). Associations between 24-h energy expenditure and fat-free mass during energy balance (A) and…
On the other hand, testosterone-dependent immunossuppression could also be the consequence of an ‘indirect pathway’ (Owen-Ashley et al. 2004) mediated by the pro-oxidant properties of this androgen, as firstly proposed by von Schantz et al. (1999). This is also in agreement with recent studies (Buchanan et al. 2001; Duckworth et al. 2001; see also Mougeot et al. 2004), which have shown that the cost of high testosterone concentration is not exclusively based on immunosuppression, as proposed by the immunocompetence handicap hypothesis (Folstad & Karter 1992). To assess the sensitivity of the results to these extreme values, we also ran the analyses excluding birds that had testosterone values higher than 20 ng ml−1. In this study, the highest value for control birds (with empty implants) was 7.66 ng ml−1, whereas the highest value for T-individuals was 35 ng ml−1. To manipulate testosterone, we used implants filled with this steroid and flutamide, a testosterone antagonist that binds to testosterone receptors. Male zebra finches whose testosterone receptors were blocked by the anti-androgen (flutamide) showed the strongest resistance to free radicals and the strongest immune response, whereas T-implanted males had the weakest resistance to free radicals and the weakest immune response.
Conversely, Bauman et al. (29) reported increases in energy expenditure under resting/fasted conditions in hypogonadal males with chronic spinal cord injury receiving 5 to 10 mg transdermal T patch daily for 12 months. Fat mass decreased similarly in TEST (−4.7 ± 1.3 kg) and PLA (−4.6 ± 1.0 kg). Normality of the data was assessed using Shapiro–Wilk tests for dependent variables.
In the present exploratory study, we aim to investigate whether the metabolic protective effects of testosterone act via modulation of the expression of key targets involved in lipid and glucose metabolism in muscle, liver and adipose tissue of cholesterol-fed Tfm mice. Despite numerical increases in protein oxidation in PLA, transcriptional regulators of branched-chain amino acid breakdown were higher during deficit compared with balance, regardless of treatment. Negative nitrogen balance during energy deficit has been shown to be the result of increased reliance on endogenous protein stores for substrate oxidation because of declines in glycogen and energy availability (47).

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