Female reproductive capacity declines dramatically in the fourth decade of life as a result of an age-related decrease in oocyte quality and quantity. The primary causes of reproductive aging and the molecular factors responsible for decreased oocyte quality remain elusive. Here, we show that aging of the female germ line is accompanied by mitochondrial dysfunction associated with decreased oxidative phosphorylation and reduced Adenosine tri-phosphate (ATP) level. Diminished expression of the enzymes responsible for CoQ production, Pdss2 and Coq6, was observed in oocytes of older females in both mouse and human. The age-related decline in oocyte quality and quantity could be reversed by the administration of CoQ10. Oocyte-specific disruption of Pdss2 recapitulated many of the mitochondrial and reproductive phenotypes observed in the old females including reduced ATP production and increased meiotic spindle abnormalities, resulting in infertility. Ovarian reserve in the oocyte-specific Pdss2-deficient animals was diminished, leading to premature ovarian failure which could be prevented by maternal dietary administration of CoQ10. We conclude that impaired mitochondrial performance created by suboptimal CoQ10 availability can drive age-associated oocyte deficits causing infertility.

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Cerebral palsy (CP) is the most common cause of severe physical disability in childhood. The precise etiological factor for the development of the majority of cases of CP has not been identified, however, prematurity is considered to be the leading identifiable risk factor. During the last decade, intrauterine infection/inflammation has been identified as the most common cause of preterm delivery and neonatal complications. When microorganisms or their products gain access to the fetus they stimulate the production of cytokines and a systemic response termed FIRS (Fetal Inflammatory Response Syndrome). Subsequently, FIRS was implicated as a cause of fetal or neonatal injury that leads to CP and chronic lung disease. Several authors found an increase in the risk for CP in infants born to mothers with clinical chorioamnionitis, especially in preterm neonates. A relationship between CP and intra-amniotic inflammation was demonstrated, intrauterine infection may lead to activation of the cytokine network which in turn can cause white matter brain damage and preterm delivery, as well as the future development of CP. This white matter insult is identified clinically as periventricular leucomalacia (PVL) which is associated with the subsequent development of impaired neurological outcomes of variable severity including CP.

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The objective of this study was to determine the effects of low-level laser light exposure on the motility of spermatozoa and on DNA damage. Thirty-three semen samples were collected for routine analysis and were classified as normospermic, oligospermic, or asthenospermic. After routine semen analysis was performed, residual semen was divided into treated and control aliquots. Treated samples were exposed to a 30-second infrared laser pulse of 50 mW/cm 2 at 905 nm, a wavelength thought to increase light-sensitive cytochrome c oxidase in the mitochondrial electron transport chain. Samples were then incubated at 37uC, and aliquots were analyzed at 30 minutes and 2 hours using computerassisted semen analysis. After incubation, 250 mL of each sample was frozen at 280uC until DNA fragmentation analysis by flow cytometry. A significant increase in motility, most prominent in oligospermic and asthenospermic samples (85% increase), was observed 30 minutes after the treatment (P , .0001). No significant increase in DNA damage compared with control samples was observed. Significant changes in sperm motion kinetics were observed. Low-level laser light exposure appears to have a positive short-term effect on the motility of treated spermatozoa and did not cause any increase in DNA damage measured at 2 hours. We conclude that some cases of asthenospermia may be related to mitochondrial dysfunction. The implications of this study in terms of future clinical applications needs further investigation.

We investigated pregnancy outcome among obese women using a prospective cohort study comparing consecutive deliveries of obese and nonobese patients. Stratified analysis, using the Mantel-Haenszel technique, was done to assess the association between obesity and the risk for cesarean delivery (CD) while controlling for confounding variables. Complete data were abstracted for 376 women, of whom 21% ( N = 79) were obese. CD rate was significantly higher among obese women (32.9% versus 18.9%; P = 0.006). Maternal obesity was associated with multiparity (odds ratio [OR] 2.97, 95% confidence interval [CI] 1.27 to 6.97; P = 0.012), fertility treatments (OR 11.3, 95% CI 2.84 to 44.89; P = 0.001), insulin-treated gestational diabetes (OR 24.55, 95% CI 2.28 to 264.08; P = 0.008), and hydramnios (OR 20.46, 95% CI 2.17 to 192.89; P = 0.008). When controlling for possible confounders, the association between maternal obesity and CD remained significant (weighted OR 2.2, 95% CI 1.2 to 4.1; P = 0.018). No significant differences were noted between the groups regarding neonatal complications. Both first and second stages of labor were longer in obese women. Obesity is a risk factor for developing gestational hypertension, insulin-treated gestational diabetes, and hydramnios. Moreover, maternal obesity is an independent risk factor for CD. Additional independent risk factors for CD were fertility treatments, insulin-treated gestational diabetes, and hydramnios. However, neonatal outcome of obese women is comparable to women with normal prepregnancy body mass index.

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