3 research outputs found

    Cylindrospermopsin-microcystin-LR combinations may induce genotoxic and histopathological damage in rats

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    Cylindrospermopsin (CYN) and microcystins (MC) are cyanotoxins that can occur simultaneously in contaminated water and food. CYN/MC-LR mixtures previously investigated in vitro showed an induction of micronucleus (MN) formation only in the presence of the metabolic fraction S9. When this is the case, the European Food Safety Authority recommends a follow up to in vivo testing. Thus, rats were orally exposed to 7.5 + 75, 23.7 + 237, and 75 + 750 μg CYN/MC-LR/kg body weight (b.w.). The MN test in bone marrow was performed, and the standard and modified comet assays were carried out to measure DNA strand breaks or oxidative DNA damage in stomach, liver, and blood cells. The results revealed an increase in MN formation in bone marrow, at all the assayed doses. However, no DNA strand breaks nor oxidative DNA damage were induced, as shown in the comet assays. The histopathological study indicated alterations only in the highest dose group. Liver was the target organ showing fatty degeneration and necrotic hepatocytes in centrilobular areas, as well as a light mononuclear inflammatory periportal infiltrate. Additionally, the stomach had flaking epithelium and mild necrosis of epithelial cells. Therefore, the combined exposure to cyanotoxins may induce genotoxic and histopathological damage in vivo.Ministerio de Economía y Competitividad AGL2015-64558-

    Hepatitis E Virus (HEV) Infection in Anti-HEV Immunoglobulin G-Carrying Patients After Successful Hepatitis C Virus Treatment: Reactivation or Reinfection?

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    Although hepatitis E virus (HEV) is regarded as a self-limiting infection and anti-HEV antibodies seem to protect against reinfection, its pathogenesis is not well established. We describe 2 cases of acute symptomatic HEV infection after hepatitis C therapy in patients carrying anti-HEV immunoglobulin G antibodies, raising 2 major questions: reactivation or reinfection

    Mutations in the Progesterone Receptor (PROGINS) May Reduce the Symptoms of Acute Hepatitis E and Protect Against Infection.

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    Mutations in the progesterone receptor (PR) gene, PROGINS, have been studied in relation to hepatitis E virus (HEV) infection. Patients with the PROGINS gene may develop a worse clinical course of hepatitis E. The aim of our study was to evaluate the influence of PROGINS on the susceptibility to and the clinical course of HEV infection in HIV patients. This study included patients with HIV who were evaluated in previous prospective studies for the prevalence and incidence of HEV. The following three groups of patients were studied: (i) never infected, (ii) past infections, and (iii) recently infected. We determined the PR genotype to evaluate the proportion of patients who were homozygous for PROGINS according to HEV infection. We also compared the proportion of PROGINS carriers with a recent HEV infection according to their symptomatology. In this study, 311 patients infected with HIV were included. Of those patients, 198 were homozygous wild type (63.7%), 91 were heterozygous (29.3%), and 22 were homozygous PROGINS (7.1%). We found that the homozygous PROGINS genotype in women was associated with a lower HEV seroprevalence. In addition, in patients with a recent HEV infection, none of those homozygous for PROGINS presented symptoms. The PROGINS mutation plays a protective role against HEV infection and is associated with subclinical infection in HIV-infected patients, particularly women
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