is not involved in energy metabolism ( Shertzer et al . 2013 ). B2m has been previously shown to be stable in high-fat diet-induced oxidative stress in adipose tissue ( Bailey-Downs et al . 2013 ), and in response to oxidative stress in the brain
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Angela L Schenewerk, Francisco Í Ramírez, Christopher Foote, Tieming Ji, Luis A Martínez-Lemus, and Rocío Melissa Rivera
Monireh Mahmoodi, Malek Soleimani Mehranjani, Seyed Mohammad Ali Shariatzadeh, Hussein Eimani, and Abdulhussein Shahverdi
has been mentioned already, EPO through the prevention of oxidative stress during transplantation will lead to a reduction of IR injury ( Soleimani et al . 2011 ). The protective effects of EPO are via the inhibition of lipid peroxidation and
T Leahy, JP Rickard, RJ Aitken, and SP de Graaf
), catalase (150 IU mL −1 ) and α-tocopherol (VIT E; 1 mM; solubilised in ethanol with a final concentration of 0.5% (v/v)) were supplemented at levels that were previously shown to counteract sperm oxidative stress in vitro ( Aitken & Clarkson 1988 , Maxwell
Paola Villani, Patrizia Eleuteri, Maria Giuseppa Grollino, Michele Rescia, Pierluigi Altavista, Marcello Spanò, Francesca Pacchierotti, and Eugenia Cordelli
the higher sensitivity of this species with respect to the others. It has been proposed that oxidative stress constitutes one of the mechanisms for creation of DNA damage in sperm, and that in humans, defective chromatine remodeling renders sperm
Michael J Bertoldo, Lydie Nadal-Desbarats, Nadine Gérard, Alexis Dubois, Patricia K Holyoake, and Christopher G Grupen
glycoproteins, glycolipids and important antioxidant constituents, may be indicative of a follicular environment that was more sensitive to oxidative stress and/or increased inflammation and cell damage ( Kolwijck et al . 2009 , Sun et al . 2012 ). All the FF
P J O'Shaughnessy, A Monteiro, P A Fowler, and I D Morris
response ( Guillouzo et al . 1984 ) though they are also secreted by other organs in response to acute injury ( Zager et al . 2012 ). Both will act to reduce oxidative stress through antioxidant action or through haem binding ( Tseng et al . 2004
S Marchiani, L Tamburrino, B Ricci, D Nosi, M Cambi, P Piomboni, G Belmonte, G Forti, M Muratori, and E Baldi
1 148 – 156 . ( doi:10.4255/mcpharmacol.09.19 ) Manza LL Codreanu SG Stamer SL Smith DL Wells KS Roberts RL Liebler DC 2004 Global shifts in protein sumoylation in response to electrophile and oxidative stress . Chemical Research
S D Johnston, N Satake, Y Zee, C López-Fernández, W V Holt, and J Gosálvez
changes in the adjacent DNA. The other region where DNA may be directly attacked due to the presence of localised oxidative stress is in close proximity to the mitochondria within the proximal midpiece at the base of the sperm head. The combined loss of
RM Sainz, RJ Reiter, JC Mayo, J Cabrera, DX Tan, W Qi, and JJ Garcia
Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.
Kristina M Adams Waldorf and Ryan M McAdams
Infection by bacteria, viruses, and parasites may lead to fetal death, organ injury, or limited sequelae depending on the pathogen. Here, we consider the role of infection during pregnancy in fetal development including placental development and function, which can lead to fetal growth restriction. The classical group of teratogenic pathogens is referred to as ‘TORCH’ (Toxoplasma gondii, others like Treponema pallidum, rubella virus, cytomegalovirus, and herpes simplex virus) but should include a much broader group of pathogens including Parvovirus B19, Varicella zoster virus, and Plasmodium falciparum to name a few. In this review, we describe the influence of different infections in utero on fetal development and the short- and long-term outcomes for the neonate. In some cases, the mechanisms used by these pathogens to disrupt fetal development are well known. Bacterial infection of the developing fetal lungs and brain begins with an inflammatory cascade resulting in cytokine injury and oxidative stress. For some pathogens like P. falciparum, the mechanisms involve oxidative stress and apoptosis to disrupt placental and fetal growth. An in utero infection may also affect the long-term health of the infant; in many cases, a viral infection in utero increases the risk of developing type 1 diabetes in childhood. Understanding the varied mechanisms employed by these pathogens may enable therapies to attenuate changes in fetal development, decrease preterm birth, and improve survival.
