Garratt Michael, Brooks Robert C
Evolution and Ecology Research Centre and School of Biological, Earth and Environmental Sciences, The University of New South Wales, Sydney, NSW 2052, Australia Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA
Evolution and Ecology Research Centre and School of Biological, Earth and Environmental Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
J Exp Biol. 2015 Jan 15;218(Pt 2):223-7. doi: 10.1242/jeb.112011. Epub 2014 Dec 18.
Male-male aggression can have a large influence on access to mates, particularly in highly territorial animals such as mice. It has been suggested that males with impaired antioxidant defence and a consequential increased susceptibility to oxidative stress may have a reduced ability to invest in aggressive behaviours, which could limit their mating opportunities and reproductive success. Oxidative stress occurs as a result of an uncontrolled over-production of reactive oxygen species (ROS) in relation to defence mechanisms (such as antioxidants), and can cause damage to a variety of different cellular components. Impairments in specific aspects of antioxidant defence, leading to oxidative stress, can limit investment in some reproductive traits in males, such as sperm quality and the production of sexual signals to attract mates. However, a direct effect of impaired antioxidant defence on aggressive behaviour has not, to our knowledge, been reported. In this study, we demonstrate that mice with experimentally elevated sensitivity to oxidative stress (through inhibition of copper-zinc superoxide dismutase, Sod1) actually show the opposite response to previous predictions. Males completely deficient in SOD1 are more aggressive than both wild-type males and males that express 50% of this antioxidant enzyme. They are also faster to attack another male. The cause of this increased aggression is unknown, but this result highlights that aggressive behaviour in mice is not highly constrained by inhibited Sod1 expression, in contrast to other reproductive traits known to be impaired in this mouse model.
雄性间的攻击行为会对获取配偶产生重大影响,尤其是在像小鼠这样具有高度领地意识的动物中。有人提出,抗氧化防御受损且因此对氧化应激敏感性增加的雄性,可能在攻击行为上投入的能力降低,这可能会限制它们的交配机会和繁殖成功率。氧化应激是由于活性氧(ROS)的产生不受控制地超过了防御机制(如抗氧化剂)的能力,从而导致对各种不同细胞成分的损伤。抗氧化防御特定方面的损伤导致氧化应激,可能会限制雄性在某些生殖特征上的投入,比如精子质量以及产生吸引配偶的性信号。然而,据我们所知,尚未有报道表明抗氧化防御受损对攻击行为有直接影响。在本研究中,我们证明,实验性地提高对氧化应激敏感性的小鼠(通过抑制铜锌超氧化物歧化酶Sod1)实际表现出与先前预测相反的反应。完全缺乏SOD1的雄性比野生型雄性以及表达该抗氧化酶50%的雄性更具攻击性。它们攻击另一只雄性的速度也更快。这种攻击性增加的原因尚不清楚,但这一结果凸显出,与已知在该小鼠模型中受损的其他生殖特征不同,小鼠的攻击行为并没有受到Sod1表达受抑制的高度限制。