A recent analysis of urine samples collected from men
A recent analysis of 2721 urine samples collected from 245 men and 408 women across the US general population between 2005 and 2010 showed that MP, PP and BuP were measurable in 99.9%, 98.3% and 73.6% of samples from women and 99.3%, 90.2% and 35.9% of samples from men, respectively (Smith et al., 2012). A study by Calafat et al. (2010) similarly detected MP (99.1%), EP (42.4%), PP (92.7%) and BuP (47%) in 2548 urine samples taken from the US general population via the 2005–2006 National Health and Nutrition Examination Survey. European studies have also demonstrated the presence of parabens in urine samples from the general population, with parabens detectable in 98% of urine samples from 60 Danish men (Frederiksen et al., 2011) and in 100% of urine samples from pregnant women and children in Spain (Casas et al., 2011). As such, the effects of parabens on the general population should also be of concern. ERRγ is expressed very strongly in a tissue-restricted manner in the mammalian placenta and foetal SNX-2112 during development, and in the brain, lung and many other tissues during adulthood (Eudy et al., 1998, Heard et al., 2000, Lorke et al., 2000). BPA is known as a strong agonist of ERRγ, and many of its neural effects have been documented, including altered explorative activity, impaired social interaction/activity, compromised learning and memory, increased anxiety and aggression, decreased male sexual behaviour, modified or lost brain sex differences, increased number of oxytocin neurones in the paraventricular nucleus, loss of sex differences in the AVPV volume and tyrosine hydroxylase levels, loss of sex difference in the locus coeruleus volume, altered nitric oxide synthase signalling and advanced puberty (Frye et al., 2012). Okada et al. (2008) suggested a strong binding of BPA to ERRγ as a reason for BPA\'s known effects on the central nervous system. Thus, the possible neurotoxicity of parabens on general populations, especially foetuses and children, deserve more attention.
Conflict of interest statement
Introduction Tissue vascular supply is tightly coupled to its oxidative capacity. This is especially evident in skeletal muscle beds enriched in either oxidative slow-twitch or glycolytic fast-twitch myofibers (Flück and Hoppeler, 2003, Pette and Staron, 2000). Slow-twitch muscles are characterized by high mitochondrial content, fatigue-resistant (type I) fibers, and dense vascularity to ensure a steady and prolonged supply of oxygen and nutrients (Annex et al., 1998, Cherwek et al., 2000, Ripoll et al., 1979). Fast-twitch (type II) muscles generally have lower oxidative capacity and a reduced blood supply and are fatigue sensitive. How the type I versus the type II muscle vasculature is specified to match oxidative capacity is unclear. Previous studies have established that nuclear receptors such as PPARα, PPARδ, and ERRα, along with coregulators PGC-1α, PGC-1β, and Rip140 control diverse aspects of aerobic respiration, including fatty acid oxidation, oxidative phosphorylation, and mitochondrial biogenesis, in skeletal muscle (Arany et al., 2007, Huss et al., 2004, Lin et al., 2002, Minnich et al., 2001, Muoio et al., 2002, Seth et al., 2007, Wang et al., 2004). While signaling factors such as TGF-β1, platelet-derived growth factor, fibroblast growth factors (FGF) 1 and 2, and vascular endothelial growth factor (VEGF) are known to stimulate angiogenesis (Carmeliet, 2000, Ferrara and Kerbel, 2005, Gustafsson and Kraus, 2001), whether and how these factors orchestrate dense vascularization of aerobic muscles is unclear. One possibility is vascular arborization by coactivator PGC-1α that is induced by hypoxia and exercise (Arany et al., 2008). However, PGC-1α knockout mice are viable, still retain oxidative muscle, and have normal vasculature (Arany et al., 2008; Lin et al., 2004). Since the intrinsic enrichment of blood flow to aerobic muscles in the absence of exercise is unlikely to depend on PGC-1α induction, we speculate the existence of an alternative regulatory angiogenic pathway.