1,721,014 research outputs found
Oestrogenic mycotoxin exposures and precocious pubertal development
No full textP>Since the 1970s, there has been a worldwide scientific discussion on the potential health consequences of human exposure to endocrine disrupters: many environmentally persistent compounds are oestrogen agonists and/or androgen antagonists. Thus, they can dysregulate the hypothalamic-pituitary-gonadal axis potentially affecting human puberty timing. Zearalenone (ZEA) is a non-steroidal mycotoxin produced by Fusarium species on several grains. Despite its low acute toxicity and carcinogenicity, ZEA exhibits oestrogenic and anabolic properties in several animal species. ZEA food contamination is caused either by direct contamination of grains, fruits and their based-products or by 'carry-over' of mycotoxins in animal tissues, milk and eggs after intake of contaminated feedstuff. In addition, zeranol (alpha-ZAL), a resorcyl lactone derived from ZEA, has been widely used in the USA as a growth promoter to improve fattening rates in cattle. From 1978 to 1984, a great epidemic of premature thelarche and precocious puberty occurred in Puerto Rico. To explain this condition, it was suggested that dairy and meat products could be contaminated with anabolic oestrogens such as ZEA or alpha-ZAL. Subsequently, worldwide other groups have also reported causative associations between oestrogenic mycotoxins and development of early thelarche and/or precocious puberty in exposed children. In addition to animal data, epidemiological studies strongly support the hypothesis that human pubertal development may be induced by foetal/early or prepubertal exposure to oestrogenic compounds. Indeed, ZEA and its metabolites are able to adopt molecular conformation, which sufficiently resembles 17 beta-oestradiol to allow it to bind to oestrogen receptors (ERs) in target cells exerting oestrogenic (agonist) actions. In this view, oestrogenic mycotoxins are suspected as triggering factor for precocious pubertal development at least in prepubertal exposed girls
Sex steroidal targets & genetic susceptibility to idiopathic cryptorchidism
No full textCryptorchidism, the most common congenital abnormality in newborn boys, is a major risk factor for male infertility and testicular malignancy in adulthood. This disorder appears as an isolated form or as part of impaired male sex development or a congenital malformation syndrome. Based mainly on the laboratory studies of the rodent models, sex steroidal signaling pathways have been shown to be involved in testicular descent; however, data on the human genetic susceptibility are less compelling. Mutations in the human genes encoding androgen receptor (AR), estrogen receptor alpha (ERalpha) and beta (ERbeta), and steroidogenic factor-1 (SF-1) have occasionally been identified but do not seem to be a frequent cause of this genital malformation. On the other hand, common polymorphisms in these genes have recently been investigated as possible contributing risk factors for idiopathic isolated (nonsyndromic) cryptorchidism, alone or by influencing susceptibility to other causal factors such as environmental endocrine disruptors. Abbreviations: Androgen Receptor (AR); DNA-Binding Domain (DBD) ;Environmental Estrogen Disruptors (EEDs); Estrogen Receptor Alpha (ERalpha); Estrogen Receptor Beta (ERbeta); Ligand-Binding Domain (LBD); Linkage Disequilibrium (LD); Odds Ratio (OR); Restriction Fragment Length Polymorphism (RFLP); Single Nucleotide Polymorphism (SNP); Steroidogenic Factor-1 (SF-1); Transactivation Domain (TAD); Testicular Dysgenesis Syndrome (TDS); Wild Type (WT)
Morphogenetic Targets and Genetics of Undescended Testis
No full textAlthough important advances in testicular physiology have been achieved, the aetiology of human cryptorchidism remains mostly unknown. Next to sex steroidal signaling pathways, morphogenetic genes are specifically involved in the testicular descent via gubernacular development. Mutations in the human genes encoding insulin-like factor 3 (INSL3) and its Leu-rich repeat-containing G protein-coupled receptor 8 (LGR8), homeobox A10 (HOXA10), zinc finger 214 (ZNF214) and 215 (ZNF215) have occasionally been identified but do not seem to be a frequent cause of cryptorchidism. On the other hand, common polymorphisms in these genes have recently been investigated as contributing risk factors for idiopathic isolated (nonsyndromic) cryptorchidism. Copyright (C) 2010 S. Karger AG, Base
Linfoadeniti da germi piogeni, mycobatteri atipici,da Mycobacterium tubercolosis, graffio di gatto, toxoplasma condii.
No full textMycoestrogen Pollution of Italian Infant Food
No full textObjective To determine the concentrations of zearalenone and its metabolites in the leading brands of infant formula milks and meat-based infant foods commonly marketed in Italy, and to assess their repercussion in the provisional tolerable daily intakes of these estrogenic mycotoxins. Study design A total of 185 cow's milk-based infant formulas and 44 samples of meat-based infant foods samples were analyzed. The analysis of mycotoxins was performed by immunoaffinity column clean-up and high-pressure liquid chromatography with fluorescence detection. Results Zearalenone was detected in 17 (9%) milk samples (maximum 0.76 mu g/L). The alpha-zearalenol was detected in 49 (26%) milk samples (maximum 12.91 mu g/L). The beta-zearalenol was detected in 53 (28%) milk samples (maximum 73.24 mu g/L). The alpha-zearalanol and beta-zearalanol were not detected in milk samples. Although a-zearalenol was detected in 12 (27%) meat samples (maximum 30.50 mu g/kg), only one meat-based sample was contaminated by alpha-zearalanol (950 mu g/kg). Zearalenone, beta-zearalenol, and beta-zearalanol were not detected in meat samples. Conclusions This study shows the presence of mycoestrogens in infant (milk-based and meat-based) food, and this is likely to have great implications for subsequent generations, suggesting the need to perform occurrence surveys in this type of food. (J Pediatr 2011; 159: 278-83)
Human breast milk and xenoestrogen exposure: a possible impact on human health.
No full textHuman milk is the best natural and optimal food for neonates with several immunologic, developmental and practical advantages throughout childhood. Although the World Health Organization strongly supports breastfeeding, it recognizes the potential health risks posed by the presence of environmental toxicants in breast milk. Contamination of human milk is widespread and due to decades of inadequately controlled pollution by toxicants, persistent pesticides or chemical solvents. These chemicals tend to degrade slowly in the environment, to bioaccumulate in the food chain and to have long half-lives in humans. Many of these environmental pollutants have estrogen-like activities and, thus they are called environmental estrogen disruptors or xenoestrogens. Certain adverse health and reproductive outcomes are attributed to these chemicals in laboratory animals and in wildlife as well as in humans. Here, we review available data from breast milk monitoring studies suggesting the environmental chemicals that may affect child health through breastfeeding
The TTTA repeats polymorphism of aromatase (CYP19) gene do not correlate with the pubarche developement in caucasian health girls
No full textGrowth Outcome during GnRH Agonist Treatments for Slowly Progressive Central Precocious Puberty
No full textBackground: Gonadotropin-releasing hormone agonists (GnRHa) represent the gold-standard treatment for central precocious puberty (CPP). In CPP children, GnRHa treatment slows bone age progression and preserves adult height (Ht) by suppressing sexual steroid secretion. In some patients, however, GnRHa induce an inappropriate growth deceleration impairing Ht outcome. Furthermore, slowly progressive CPP (spCPP) forms were reported which do not need GnRHa treatment. Methods: We evaluated the growth outcome of 26 spCPP girls treated with triptorelin (TR) and 21 with leuprorelin acetate (LA) for 36.5 +/- 0.7 months. Results: GnRHa treatment induced a progressive growth deceleration in both spCPP groups. No difference in bone maturation was detected (p > 0.05; TR vs. LA group), however compared to LA, TR treatment resulted in significantly higher Ht after 24 months (p 0.05; LA vs. TR group), final height (FH-SDS) was lower in LA-treated subjects (p < 0.05; LA vs. TR group). In both spCPP groups, FH-SDS was significantly lower than TH-SDS (p < 0.001) but not lower than PAH-SDS at diagnosis (p 1 0.05). Ht-SDS correlated with 17 beta-estradiol (E(2)) blood levels in both spCPP groups (p < 0.0001) throughout GnRHa treatment, and E(2) values were higher in the TR- than in the LA-treated patients during the 12 months after GnRHa administration (p < 0.05; LA vs. TR group). GnRHa-induced E(2) secretion and Ht-SDS at GnRHa withdrawal correlated positively with FH (p < 0.01 and p < 0.001, respectively). Conclusions: The effectiveness of GnRHa treatment in improving FH in spCPP girls was doubtful. Copyright (C) 2009 S. Karger AG, Base
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