{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T02:32:33Z","timestamp":1791772353368,"version":"4.3.4"},"reference-count":84,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,9,12]],"date-time":"2020-09-12T00:00:00Z","timestamp":1599868800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Cancer is associated with muscle atrophy (cancer cachexia) that is linked to up to 40% of cancer\u2010related deaths. Oxidative stress is a critical player in the induction and progression of age\u2010related loss of muscle mass and weakness (sarcopenia); however, the role of oxidative stress in cancer cachexia has not been defined. The purpose of this study was to examine if elevated oxidative stress exacerbates cancer cachexia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Cu\/Zn superoxide dismutase knockout (Sod1KO) mice were used as an established mouse model of elevated oxidative stress. Cancer cachexia was induced by injection of one million Lewis lung carcinoma (LLC) cells or phosphate\u2010buffered saline (saline) into the hind flank of female wild\u2010type mice or Sod1KO mice at approximately 4\u00a0months of age. The tumour developed for 3\u00a0weeks. Muscle mass, contractile function, neuromuscular junction (NMJ) fragmentation, metabolic proteins, mitochondrial function, and motor neuron function were measured in wild\u2010type and Sod1KO saline and tumour\u2010bearing mice. Data were analysed by two\u2010way ANOVA with Tukey\u2013Kramer post hoc test when significant\n                      <jats:italic>F<\/jats:italic>\n                      ratios were determined and\n                      <jats:italic>\u03b1<\/jats:italic>\n                      was set at 0.05. Unless otherwise noted, results in abstract are mean \u00b1SEM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Muscle mass and cross\u2010sectional area were significantly reduced, in tumour\u2010bearing mice. Metabolic enzymes were dysregulated in Sod1KO mice and cancer exacerbated this phenotype. NMJ fragmentation was exacerbated in tumour\u2010bearing Sod1KO mice. Myofibrillar protein degradation increased in tumour\u2010bearing wild\u2010type mice (wild\u2010type saline, 0.00847\u00a0\u00b1\u00a00.00205; wildtype LLC, 0.0211\u00a0\u00b1\u00a00.00184) and tumour\u2010bearing Sod1KO mice (Sod1KO saline, 0.0180\u00a0\u00b1\u00a00.00118; Sod1KO LLC, 0.0490\u00a0\u00b1\u00a00.00132). Muscle mitochondrial oxygen consumption was reduced in tumour\u2010bearing mice compared with saline\u2010injected wild\u2010type mice. Mitochondrial protein degradation increased in tumour\u2010bearing wild\u2010type mice (wild\u2010type saline, 0.0204\u00a0\u00b1\u00a00.00159; wild\u2010type LLC, 0.167\u00a0\u00b1\u00a00.00157) and tumour\u2010bearing Sod1KO mice (Sod1KO saline, 0.0231\u00a0\u00b1\u00a00.00108; Sod1 KO LLC, 0.0645\u00a0\u00b1\u00a00.000631). Sciatic nerve conduction velocity was decreased in tumour\u2010bearing wild\u2010type mice (wild\u2010type saline, 38.2\u00a0\u00b1\u00a00.861; wild\u2010type LLC, 28.8\u00a0\u00b1\u00a00.772). Three out of eleven of the tumour\u2010bearing Sod1KO mice did not survive the 3\u2010week period following tumour implantation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Oxidative stress does not exacerbate cancer\u2010induced muscle loss; however, cancer cachexia may accelerate NMJ disruption.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcsm.12615","type":"journal-article","created":{"date-parts":[[2020,9,18]],"date-time":"2020-09-18T03:22:22Z","timestamp":1600399342000},"page":"1688-1704","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["Cancer cachexia in a mouse model of oxidative stress"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0912-7924","authenticated-orcid":false,"given":"Jacob 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