Michalkova Veronika, Benoit Joshua B, Attardo Geoffrey M, Medlock Jan, Aksoy Serap
Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut, United State of America; Section of Molecular and Applied Zoology, Institute of Zoology, Slovak Academy of Sciences, Bratislava, Slovakia.
Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut, United State of America.
PLoS One. 2014 Apr 24;9(4):e87554. doi: 10.1371/journal.pone.0087554. eCollection 2014.
Impact of reproductive processes upon female health has yielded conflicting results; particularly in relation to the role of reproduction-associated stress. We used the viviparous tsetse fly to determine if lactation, birth and involution lead to damage from oxidative stress (OS) that impairs subsequent reproductive cycles. Tsetse females carry an intrauterine larva to full term at each pregnancy cycle, and lactate to nourish them with milk secretions produced by the accessory gland ( = milk gland) organ. Unlike most K-strategists, tsetse females lack an apparent period of reproductive senescence allowing the production of 8-10 progeny over their entire life span. In a lactating female, over 47% of the maternal transcriptome is associated with the generation of milk proteins. The resulting single larval offspring weighs as much as the mother at birth. In studying this process we noted an increase in specific antioxidant enzyme (AOE) transcripts and enzymatic activity at critical times during lactation, birth and involution in the milk gland/fat body organ and the uterus. Suppression of superoxide dismutase (sod) decreased fecundity in subsequent reproductive cycles in young mothers and nearly abolished fecundity in geriatric females. Loss of fecundity was in part due to the inability of the mother to produce adequate milk to support larval growth. Longevity was also impaired after sod knockdown. Generation of OS in virgin females through exogenous treatment with hydrogen peroxide at times corresponding to pregnancy intervals reduced survival, which was exacerbated by sod knockdown. AOE expression may prevent oxidative damage associated with the generation of nutrients by the milk gland, parturition and milk gland breakdown. Our results indicate that prevention of OS is essential for females to meet the growing nutritional demands of juveniles during pregnancy and to repair the damage that occurs at birth. This process is particularly important for females to remain fecund during the latter portion of their lifetime.
生殖过程对女性健康的影响产生了相互矛盾的结果;特别是在与生殖相关压力的作用方面。我们利用胎生采采蝇来确定泌乳、分娩和 involution 是否会导致氧化应激(OS)造成损害,从而损害后续的生殖周期。采采蝇雌性在每个妊娠周期都会将子宫内的幼虫孕育至足月,并通过乳腺(=乳腺)器官分泌的乳汁来哺育幼虫。与大多数 K 策略者不同,采采蝇雌性没有明显的生殖衰老期,能够在其整个生命周期中产下 8 - 10 只后代。在泌乳期雌性中,超过 47% 的母体转录组与乳蛋白的生成相关。出生时,单个幼虫后代的体重与母亲相当。在研究这个过程中,我们注意到在泌乳、分娩和 involution 期间的关键时间点,乳腺/脂肪体器官和子宫中特定抗氧化酶(AOE)的转录本和酶活性有所增加。超氧化物歧化酶(sod)的抑制降低了年轻母亲后续生殖周期的繁殖力,而在老年雌性中几乎消除了繁殖力。繁殖力的丧失部分是由于母亲无法分泌足够的乳汁来支持幼虫生长。sod 敲低后,寿命也受到了损害。在与妊娠间隔相对应的时间对外源过氧化氢处理处女雌性,会导致 OS 的产生,从而降低存活率,sod 敲低会加剧这种情况。AOE 的表达可能会预防与乳腺产生营养物质、分娩和乳腺分解相关的氧化损伤。我们的结果表明,预防 OS 对于雌性在怀孕期间满足幼体不断增长的营养需求以及修复出生时发生的损伤至关重要。这个过程对于雌性在其生命周期后期保持生育能力尤为重要。