The role of steroids in carcinogenesis has become a major concern in environmental protection, biomonitoring, and clinical research. Although historically oestrogen has been related to development of reproductive system, research over the last decade has confirmed its crucial role in the development and homeostasis of other organ systems. As a number of anthropogenic agents are xenoestrogens, environmental health research has focused on oestrogen receptor level disturbances and of aromatase polymorphisms. Oestrogen and xenoestrogens mediate critical points in carcinogenesis by binding to oestrogen receptors, whose distribution is age-, gender-, and tissue-specific. This review brings data about cancer types whose eatiology may be found in environmental exposure to xenoestrogens. Cancer types that have been well documented in literature to be related with environmental exposure include the reproductive system, breast, lung, kidney, pancreas, and brain. The results of our data mining show (a) a significant correlation between exposure to xenoestrogens and increased, gender-related, cancer risk and (b) a need to re-evaluate agents so far defined as endocrine disruptors, as they are also key molecules in carcinogenesis. This revision may be used to further research of cancer aetiology and to improvement of related legislation. Investigation of cancers caused by xenoestrogens may elucidate yet unknown mechanisms also valuable for oncology and the development of new therapies.

The cell adhesion molecule close homolog of L1 (CHL1) plays important functional roles in the developing and adult nervous system. In search of the binding partners that mediate the diverse and sometimes opposing functions of CHL1, the extracellular matrix-associated proteins vitronectin and plasminogen activator inhibitor-2 (PAI-2) were identified as novel CHL1 interaction partners and tested for involvement in CHL1-dependent functions during mouse cerebellar development. CHL1-induced cerebellar neurite outgrowth and cell migration at postnatal days 6 -8 were inhibited by a CHL1-derived peptide comprising the integrin binding RGD motif, and by antibodies against vitronectin or several integrins, indicating a vitronectin-dependent integrin-mediated pathway. A PAI-2-derived peptide, or antibodies against PAI-2, urokinase type plasminogen activator (uPA), uPA receptor, and several integrins reduced cell migration. CHL1 colocalized with vitronectin, PAI-2, and several integrins in cerebellar granule cells, suggesting an association among these proteins. Interestingly, at the slightly earlier age of 4 -5 d, cerebellar neurons did not depend on CHL1 for neuritogenesis and cell migration. However, differentiation of progenitor cells into neurons at this stage was dependent on homophilic CHL1-CHL1 interactions. These observations indicate that homophilic CHL1 trans-interactions regulate differentiation of neuronal progenitor cells at early postnatal stages, while heterophilic trans-interactions of CHL1 with vitronectin, integrins, and the plasminogen activator system regulate neuritogenesis and neuronal cell migration at a later postnatal stage of cerebellar morphogenesis. Thus, within very narrow time windows in postnatal cerebellar development, distinct types of molecular interactions mediated by CHL1 underlie the diverse functions of this protein.

ProblemThe issue of the present and past roles of sea turtles in ecosystems is underlined as one of the global research priorities for sea turtle management and conservation in the 21st century (Hamann et al. 2010). Sea turtles act at multiple levels, as predators, prey, competitors, substrate for epibionts, hosts of parasites and pathogens, nutrient transporters and modifiers of habitats (Bjorndal 2003;Bjorndal & Jackson 2003). Knowledge on the role of sea turtles in the ecosystems they utilize is necessary for our ability to predict how natural and anthropogenic-driven environmental changes can affect their populations in order to make informed management decisions (Bjorndal 2003).Loggerhead sea turtle, Caretta caretta (Linnaeus, 1758) is an endangered (IUCN 2009), large, long-lived top predator in marine ecosystems, with a complex life history characterised by switching between different habitats AbstractMolluscs are a diverse and ubiquitous group of organisms which contribute to the formation of biogenic sediments and are one of the major prey taxa for the neritic-stage loggerhead sea turtles (Caretta caretta) worldwide. Here we investigated to what degree molluscs contribute to the diet of individual turtles, and what role the feeding strategy of loggerheads might play in bioturbation, one of the key processes in nutrient transport in marine ecosystems. We performed a detailed analysis of benthic molluscs from the digestive tracts of 62 loggerhead sea turtles (curved carapace length: 25.0-85.4 cm) found in the Northern Adriatic Sea. From 50 of the turtles that contained benthic molluscs, we identified 87 species representing 40 families and three classes (Gastropoda, Bivalvia and Scaphopoda), including 72 new dietary records for loggerhead turtle. Most of the identified molluscs were small-sized species (shell length £ 3 cm) and were often found in a subfossil condition. Their intake may be considered a byproduct of infaunal mining, while larger molluscs were mainly found crushed into smaller fragments. Through such foraging behaviour loggerheads actively rework sediments, increase the surface area of shells and the rate of shells disintegration, acting as bioturbators in this system. We conservatively estimate that loggerheads in the neritic zone of the Adriatic Sea bioturbate about 33 tonnes of mollusc shells per year, and hypothesize about the possible effects of bioturbation reduction on environmental changes in the Northern Adriatic ecosystem.

The serotonergic system plays important roles in multiple functions of the nervous system and its malfunctioning leads to neurological and psychiatric disorders. Here, we show that the cell adhesion molecule close homolog of L1 (CHL1), which has been linked to mental disorders, binds to a peptide stretch in the third intracellular loop of the serotonin 2c (5-HT2c) receptor through its intracellular domain. Moreover, we provide evidence that CHL1 deficiency in mice leads to 5-HT2c-receptor-related reduction in locomotor activity and reactivity to novelty, and that CHL1 regulates signaling pathways triggered by constitutively active isoforms of the 5-HT2c receptor. Furthermore, we found that the 5-HT2c receptor and CHL1 colocalize in striatal and hippocampal GABAergic neurons, and that 5-HT2c receptor phosphorylation and its association with phosphatase and tensin homolog (PTEN) and β-arrestin 2 is regulated by CHL1. Our results demonstrate that CHL1 regulates signal transduction pathways through constitutively active 5-HT2c receptor isoforms, thereby altering 5-HT2c receptor functions and implicating CHL1 as a new modulator of the serotonergic system.