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Sex-specific effects of inbreeding and early ife conditions on the adult oxidative balance 被引量:2
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作者 Raissa Anna DE BOER David COSTANTINI +4 位作者 Giulia CASASOLE Hamada ABDELGAWAD Han ASARD Marcel EENS Wendt MIJLLER 《Current Zoology》 SCIE CAS CSCD 2018年第5期631-639,共9页
Inbreeding negatively affects various life-history traits, with inbred individuals typically having lower fit- ness than outbred individuals (=inbreeding depression). Inbreeding depression is often emphasized under ... Inbreeding negatively affects various life-history traits, with inbred individuals typically having lower fit- ness than outbred individuals (=inbreeding depression). Inbreeding depression is often emphasized under environmental stress, but the underlying mechanisms and potential long-lasting consequences of such inbreeding-environment interactions remain poorly understood. Here, we hypothesize that inbreeding-environment interactions that occur early in life have long-term physiological effects, in partic- ular on the adult oxidative balance. We applied a unique experimental design to manipulate early life conditions of inbred and outbred songbirds (Serinus canaria) that allowed us to separate prenatal and postnatal components of early life conditions and their respective importance in inbreeding-environment interactions. We measured a wide variety of markers of oxidative status in adulthood, resulting in a com- prehensive account for oxidative balance. Using a Bayesian approach with Markov chain Monte Carlo, we found clear sex-specific effects and we also found only in females small yet significant long-term effects of inbreeding-environment interactions on adult oxidative balance. Postnatal components of early life conditions were most persuasively reflected on adult oxidative balance, with inbred females that experienced disadvantageous postnatal conditions upregulating enzymatic antioxidants in adulthood. Our study provides some evidence that adult oxidative balance can reflect inbreeding-environment inter- actions early in life, but given the rather small effects that were limited to females, we conclude that oxida- tive stress miaht have a limited role as mechanism underlvina inhre.e.dina-envirnnme.nt inte.raetinn.q_ 展开更多
关键词 CANARY maternal effects gene-environment interactions hatching asynchrony.
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Oxidative stress favours herpes virus infection in vertebrates: a meta-analysis
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作者 Manrico SEBASTIANO Olivier CHASTEL +2 位作者 Benoit DE THOBY Marcel EENS David COSTANTINI 《Current Zoology》 SCIE CAS CSCD 2016年第4期325-332,共8页
Herpes viruses are responsible for a variety of pathological effects in humans and in both wild and domestic animals. One mechanism that has been proposed to facilitate replication and activity of herpes viruses is ox... Herpes viruses are responsible for a variety of pathological effects in humans and in both wild and domestic animals. One mechanism that has been proposed to facilitate replication and activity of herpes viruses is oxidative stress (OS). We used meta-analytical techniques to test the hypotheses that (1) herpes virus infection causes OS and (2) supplementation of antioxidants reduces virus load, indicating that replication is favoured by a state of OS. Results based on studies on mammals, including humans, and birds show that (1) OS is indeed increased by herpes virus infection across multiple tissues and species, (2) biomarkers of OS may change differently between tissues, and (3) the effect size does not differ among different virus strains. In addition, the increase of oxidative damage in blood (tissue commonly available in ecological studies) was similar to that in the tissues most sensitive to the herpes virus. Our results also show that administration of antioxidants re- duces virus yield, indicating that a condition of OS is favorable for the viral replication. In addition, some antioxidants may be more efficient than others in reducing herpes virus yield. Our results point to a potential mechanism linking herpes virus infection to individual health status. 展开更多
关键词 ANTIOXIDANTS herpes virus infection immune response interaction host-pathogen oxidative stress.
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