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      Protective effects of Coridius chinensis extracts on rat reproductive damage induced by manganese

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          Abstract

          Manganese (Mn 2+) is an environmental pollutant, and testis is one of the main target organs. Coridius chinensis ( C. chinensis), a traditional Chinese medicine, has been shown widely used in treating various kinds of pain, nephropathy and erectile dysfunction. In our recent study, we found that Mn 2+ exposure caused testicular injury could be rescued in part by the antioxidant activity of C. chinensis extracts (CcE). However, there is dearth of extensive knowledge on the therapeutic effects of C. chinensis on manganese‐induced reproductive toxicity. In the present study, Sprague‐Dawley (SD) rats were administered manganese chloride alone or co‐treated with CcE for 30 consecutive days. Results indicated that C. chinensis mediated suppression of spermatogenic dysfunction, and the number of apoptotic cells was significantly decreased in CcE‐treated groups. Furthermore, the disintegrated testicular ultrastructural structure caused by Mn 2+ was partially repaired in CcE‐treated groups. C. chinensis significantly inhibited Mn 2+‐induced decline in biomarkers of blood–testis barrier (BTB) including occludin, claudin1, zonula occludens‐1 and junctional adhesion molecule 1, whereas it decreased the expression of focal adhesion kinase (FAK) and c‐Src. This study demonstrated that c‐Src and FAK might be involved in the repair of Mn 2+‐induced testicular injury by C. chinensis, but further research is needed.

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          Nutritional aspects of manganese homeostasis.

          Manganese (Mn) is an essential mineral. It is present in virtually all diets at low concentrations. The principal route of intake for Mn is via food consumption, but in occupational cohorts, inhalation exposure may also occur (this subject will not be dealt with in this review). Humans maintain stable tissue levels of Mn. This is achieved via tight homeostatic control of both absorption and excretion. Nevertheless, it is well established that exposure to high oral, parenteral or ambient air concentrations of Mn can result in elevations in tissue Mn levels. Excessive Mn accumulation in the central nervous system (CNS) is an established clinical entity, referred to as manganism. It resembles idiopathic Parkinson's disease (IPD) in its clinical features, resulting in adverse neurological effects both in laboratory animals and humans. This review focuses on an area that to date has received little consideration, namely the potential exposure of parenterally fed neonates to exceedingly high Mn concentrations in parenteral nutrition solutions, potentially increasing their risk for Mn-induced adverse health sequelae. The review will consider (1) the essentiality of Mn; (2) the concentration ranges, means and variation of Mn in various foods and infant formulas; (3) the absorption, distribution, and elimination of Mn after oral exposure and (4) the factors that raise a theoretical concern that neonates receiving total parenteral nutrition (TPN) are exposed to excessive dietary Mn.
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            The blood-testis barrier and its implications for male contraception.

            The blood-testis barrier (BTB) is one of the tightest blood-tissue barriers in the mammalian body. It divides the seminiferous epithelium into the basal and the apical (adluminal) compartments. Meiosis I and II, spermiogenesis, and spermiation all take place in a specialized microenvironment behind the BTB in the apical compartment, but spermatogonial renewal and differentiation and cell cycle progression up to the preleptotene spermatocyte stage take place outside of the BTB in the basal compartment of the epithelium. However, the BTB is not a static ultrastructure. Instead, it undergoes extensive restructuring during the seminiferous epithelial cycle of spermatogenesis at stage VIII to allow the transit of preleptotene spermatocytes at the BTB. Yet the immunological barrier conferred by the BTB cannot be compromised, even transiently, during the epithelial cycle to avoid the production of antibodies against meiotic and postmeiotic germ cells. Studies have demonstrated that some unlikely partners, namely adhesion protein complexes (e.g., occludin-ZO-1, N-cadherin-β-catenin, claudin-5-ZO-1), steroids (e.g., testosterone, estradiol-17β), nonreceptor protein kinases (e.g., focal adhesion kinase, c-Src, c-Yes), polarity proteins (e.g., PAR6, Cdc42, 14-3-3), endocytic vesicle proteins (e.g., clathrin, caveolin, dynamin 2), and actin regulatory proteins (e.g., Eps8, Arp2/3 complex), are working together, apparently under the overall influence of cytokines (e.g., transforming growth factor-β3, tumor necrosis factor-α, interleukin-1α). In short, a "new" BTB is created behind spermatocytes in transit while the "old" BTB above transiting cells undergoes timely degeneration, so that the immunological barrier can be maintained while spermatocytes are traversing the BTB. We also discuss recent findings regarding the molecular mechanisms by which environmental toxicants (e.g., cadmium, bisphenol A) induce testicular injury via their initial actions at the BTB to elicit subsequent damage to germ-cell adhesion, thereby leading to germ-cell loss, reduced sperm count, and male infertility or subfertility. Moreover, we also critically evaluate findings in the field regarding studies on drug transporters in the testis and discuss how these influx and efflux pumps regulate the entry of potential nonhormonal male contraceptives to the apical compartment to exert their effects. Collectively, these findings illustrate multiple potential targets are present at the BTB for innovative contraceptive development and for better delivery of drugs to alleviate toxicant-induced reproductive dysfunction in men.
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              Tyrosine phosphorylation and dissociation of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the cytoskeleton by oxidative stress.

              The oxidative-stress-induced alteration in paracellular junctional complexes was analysed in Caco-2 cell monolayer. Oxidative stress induced a rapid increase in tyrosine phosphorylation of occludin, zonula occludens (ZO)-1, E-cadherin and beta-catenin. An oxidative-stress-induced decrease in transepithelial electrical resistance was associated with a redistribution of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the intercellular junctions. Genistein, a tyrosine kinase inhibitor, prevented the oxidative-stress-induced decrease in resistance and redistribution of protein complexes. Occludin, ZO-1, E-cadherin and beta-catenin in the Triton-insoluble cytoskeletal fraction were reduced by oxidative stress, which was prevented by genistein. Oxidative stress also reduced the co-immunoprecipitation of ZO-1 with occludin, which was prevented by genistein. Co-immunoprecipitation of beta-catenin with E-cadherin was unaffected by oxidative stress or genistein. ZO-1, E-cadherin and beta-catenin in the plasma membrane or membrane-cytoskeleton were either slightly reduced or unaffected by oxidative stress or genistein. These results show that oxidative stress induces tyrosine phosphorylation and cellular redistribution of occludin-ZO-1 and E-cadherin-beta-catenin complexes by a tyrosine-kinase-dependent mechanism.
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                Author and article information

                Contributors
                hxh19801122@163.com
                Journal
                Andrologia
                Andrologia
                10.1111/(ISSN)1439-0272
                AND
                Andrologia
                John Wiley and Sons Inc. (Hoboken )
                0303-4569
                1439-0272
                24 November 2021
                March 2022
                : 54
                : 2 ( doiID: 10.1111/and.v54.2 )
                : e14326
                Affiliations
                [ 1 ] Department of Cell Biology Zunyi Medical University Zunyi China
                Author notes
                [*] [* ] Correspondence

                Xiaohui Hou, Department of Cell Biology, Zunyi Medical University, Zunyi, China.

                Email: hxh19801122@ 123456163.com

                Author information
                https://orcid.org/0000-0002-7713-2808
                Article
                AND14326
                10.1111/and.14326
                9285684
                34820869
                a6e1b2b0-edf7-47da-a301-00acbcfe143f
                © 2021 The Authors. Andrologia published by Wiley‐VCH GmbH

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 22 October 2021
                : 01 July 2021
                : 04 November 2021
                Page count
                Figures: 7, Tables: 1, Pages: 11, Words: 6341
                Funding
                Funded by: Department of Education of Guizhou Province , doi 10.13039/501100010828;
                Award ID: [2014] 031
                Funded by: Bureau of Science and Technology of Zunyi City
                Award ID: Zunshi Kehe HZ (2019) 6
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                March 2022
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.1.7 mode:remove_FC converted:15.07.2022

                apoptosis,blood‐testis barrier,coridius chinensis,hplc,manganese

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