{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T16:31:05Z","timestamp":1792168265986,"version":"4.4.0"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2011,11,3]],"date-time":"2011-11-03T00:00:00Z","timestamp":1320278400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Hepatology Research"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p><jats:bold>Aim:\u2002<\/jats:bold> Liver injuries induced by carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>) cause mitochondrial stress and disruption of membrane potential resulting in apoptosis. In this study, we evaluated the effects of <jats:italic>Ganoderma lucidum<\/jats:italic> against CCl<jats:sub>4<\/jats:sub> (1:5 v\/v in paraffin oil, 1.5\u2003mL\/kg, i.p) induced deterioration of the activities of mitochondrial enzymes and electron transport chain complexes in the liver mitochondria.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold>  <jats:italic>Ganoderma lucidum<\/jats:italic> (100 and 250\u2003mg\/kg) was administered once daily for 15\u2003days prior to the CCl<jats:sub>4<\/jats:sub> administration. \u03b1\u2010Tocopherol (100\u2003mg\/kg, p.o.) was used as the standard. Hepatic damage was assessed by determining the activities of serum transaminases (SGPT and SGOT) and alkaline phosphatase (ALP), 24\u2003h after CCl<jats:sub>4<\/jats:sub> injection. The activities of mitochondrial dehydrogenases as well as mitochondrial complexes I, II, III, and IV were evaluated.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Activities of SGPT, SGOT and ALP were significantly (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.01) elevated whereas, the activities of mitochondrial enzymes were significantly (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.01) decreased by the CCl<jats:sub>4<\/jats:sub> challenge. The mitochondrial reactive oxygen species level was enhanced and mitochondrial membrane potential was declined significantly. Administration of <jats:italic>G.\u2003lucidum<\/jats:italic> significantly and dose independently protected liver mitochondria.<\/jats:p><jats:p><jats:bold>Conclusion:\u2002<\/jats:bold> The findings suggest that protective effect of <jats:italic>G.\u2003lucidum<\/jats:italic> against hepatic damage could be mediated by ameliorating the oxidative stress; restoring the mitochondrial enzyme activities and membrane potential.<\/jats:p>","DOI":"10.1111\/j.1872-034x.2011.00906.x","type":"journal-article","created":{"date-parts":[[2011,11,4]],"date-time":"2011-11-04T01:31:24Z","timestamp":1320370284000},"page":"181-191","source":"Crossref","is-referenced-by-count":17,"title":["<i>Ganoderma lucidum<\/i> protects liver mitochondrial oxidative stress and improves the activity of electron transport chain in carbon tetrachloride intoxicated rats"],"prefix":"10.1111","volume":"42","author":[{"given":"Narayana Panicker","family":"Sudheesh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thekuttuparambil Ananthanarayanan","family":"Ajith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John","family":"Mathew","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nalin","family":"Nima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kainoor Krishnankutty","family":"Janardhanan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,11,3]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0748-5514(85)90026-1"},{"key":"e_1_2_6_3_2","doi-asserted-by":"crossref","unstructured":"RecknagelRO GlenderEAJr BrittonRS.Free radical damage and lipid peroxidation. 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