{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T02:17:15Z","timestamp":1783477035200,"version":"3.55.0"},"reference-count":36,"publisher":"CSIRO Publishing","issue":"10","license":[{"start":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T00:00:00Z","timestamp":1782086400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/doi.org\/10.1071\/journalslicense"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,10]]},"abstract":"<jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>Heat stress (HS) induces spermatogenic disorders and reduces sperm quality in males. Alginate oligosaccharides (AOS) exhibit antioxidant and reproductive protective effects, but the molecular mechanism by which AOS improves HS-induced declines in semen quality remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>To investigate the protective effects and underlying molecular mechanism of AOS on HS-induced male reproductive impairment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Six-week-old mice were assigned to the following four groups: control, heat stress, AOS, and AOS\u00a0+\u00a0heat stress. We systematically evaluated male fertility, sperm quality, testicular morphology, blood\u2013testis barrier (BTB), tight junctions in Sertoli cells (TJs), and autophagy levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key results<\/jats:title>\n                    <jats:p>The results showed that AOS significantly attenuated the HS-induced reductions in pregnancy rate, litter size, sperm concentration, motility, and acrosome integrity. AOS also alleviated HS-induced testicular structural damage and blood\u2013testis barrier leakage, and restored the expression levels of ZO-1, occludin, and claudin-11. In addition, HS induced abnormally elevated autophagy, as evidenced by increased autophagosomes, upregulated expression of LC3B, Beclin-1, and autophagy-related genes, and decreased p62 expression levels, whereas AOS restored autophagic flux to normal levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The protective effects of AOS relieve heat stress-induced damage to tight junctions via regulating autophagy in Sertoli cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Implications<\/jats:title>\n                    <jats:p>These findings provide a theoretical basis for AOS as a potential agent for the prevention of HS-related reproductive disorders.<\/jats:p>\n                  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