Zearalenone ELISA Kit

The impact of zearalenone (ZEN) on female reproduction remains an issue, since its effects may differ among exposed cell types. Besides the use of decontaminants in animal diet, other approaches should be considered to minimise ZEN effects after exposure. Since the first organ in contact with ZEN is the gastrointestinal tract, we hypothesise that products of microbiota metabolism may play a role in ZEN detoxification. We aimed to evaluate the effect of 1 mu mol/L ZEN and 1 mu mol/L equol (a microbial metabolite), alone or in combination, on the survival and morphology of in vitro cultured ovarian preantral follicles. Ovaries from 12 sheep were collected at a local abattoir and fragmented, and the ovarian pieces were submitted to in vitro culture for three days in the presence or absence of the test compounds. The follicular morphology was impaired by ZEN, but equol could alleviate the observed degeneration rates. While ZEN decreased cell proliferation in primary and secondary follicles, as well as induced DNA double-strand breaks in primordial follicles, all these observations disappeared when equol was added to a culture medium containing ZEN. In the present culture conditions, equol was able to counteract the negative effects of ZEN on ovarian preantral follicles.

Background: The terminology of "sick building syndrome" (SBS), meaning that a person may feel sick in a certain building, but when leaving the building, the symptoms will reverse, is imprecise. Many different environmental hazards may cause the feeling of sickness, such as high indoor air velocity, elevated noise, low or high humidity, vapors or dust. The Aim: To describe SBS in connection with exposure to indoor air dampness microbiota (DM). Methods: A search through Medline/Pubmed. Results and Conclusions: Chronic course of SBS may be avoided. By contrast, persistent or cumulative exposure to DM may make SBS potentially life-threatening and lead to irreversible dampness and mold hypersensitivity syndrome (DMHS). The corner feature of DMHS is acquired by dysregulation of the immune system in the direction of hypersensitivities (types I-IV) and simultaneous deprivation of immunity that manifests as increased susceptibility to infections. DMHS is a systemic low-grade inflammation and a biotoxicosis. There is already some evidence that DMHS may be linked to autoimmunity. Autoantibodies towards, e.g., myelin basic protein, myelin-associated glycoprotein, ganglioside GM1, smooth muscle cells and antinuclear autoantibodies were reported in mold-related illness. DMHS is also a mitochondropathy and endocrinopathy. The association of autoimmunity with DMHS should be confirmed through cohort studies preferably using chip-based technology.