Testosterone and oxidative stress: the oxidation handicap hypothesis

Area of Science:

• Animal behavior
• Evolutionary endocrinology
• Physiological ecology

Background:

• Secondary sexual traits (SST) signal male quality, with honesty often linked to costly physiological trade-offs.
• The immunocompetence handicap hypothesis suggests testosterone-mediated immunosuppression ensures honest signaling.
• However, testosterone's costs may extend beyond immunity to other physiological functions, like antioxidant capacity.

Purpose of the Study:

• To investigate if testosterone compromises antioxidant defenses in a species with testosterone-dependent sexual traits.
• To test the hypothesis that testosterone depresses resistance to oxidative stress in male zebra finches.

Main Methods:

• Male zebra finches received implants of flutamide (anti-androgen), testosterone, or empty controls.
• Assessed red blood cell resistance to oxidative stress (free radical attack).
• Measured cell-mediated immune response.

Main Results:

• Testosterone-treated males exhibited the lowest red blood cell resistance to oxidative stress.
• Flutamide-treated males showed the highest resistance.
• Testosterone also depressed cell-mediated immune response, supporting the immunocompetence handicap hypothesis.

Conclusions:

• Testosterone imposes costs on antioxidant defenses, in addition to potentially suppressing immunity.
• These findings suggest a trade-off between sexual signaling benefits and the physiological costs of oxidative stress.
• Oxidative stress may be a significant cost maintaining the honesty of testosterone-based sexual signals.