{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T18:42:40Z","timestamp":1784054560362,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,11,29]],"date-time":"2007-11-29T00:00:00Z","timestamp":1196294400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Gene Medicine"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Oxidative stress, often in association with decreased antioxidant defenses, plays a pathogenetic role in both initiation and progression of liver injuries, leading to almost all clinical and experimental conditions of chronic liver diseases. Human paraoxonase 1 (hPON1) is a liver\u2010synthesized enzyme possessing antioxidant properties. Here, we investigate the effects of transgene\u2010expressed hPON1 Q on alleviating lipid peroxidation and preventing liver injury in a mouse model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The hPON1 Q gene was cloned into pcDNA3.0 plasmid and electro\u2010transferred into mouse skeletal muscle. After CCl<jats:sub>4<\/jats:sub> had been administrated to induce liver injury, mice were monitored for serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malonyldialdehyde (MDA). The extent of CCl<jats:sub>4<\/jats:sub>\u2010induced liver injury was also analyzed through histopathological observations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>After gene delivery, hPON1 mRNA expression was detected in mouse muscle and serum PON1 activity was 1.5 times higher than that of the control counterpart. In the PON1 Q gene transferred mice, protection against CCl<jats:sub>4<\/jats:sub>\u2010induced liver injury was reflected by significantly decreased serum ALT, AST and MDA levels compared to those in control mice (<jats:italic>P<\/jats:italic> &lt; 0.01). Histological observations also revealed that hepatocyte necrosis, hemorrhage, vacuolar change and hydropic degeneration were apparent in control mice after CCl<jats:sub>4<\/jats:sub> administration. In contrast, the damage was significantly prevented (<jats:italic>P<\/jats:italic> &lt; 0.01) in the hPON1 Q transferred mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Intramuscular electro\u2010transfer of the hPON1 Q gene led to efficient expression of hPON1 in mice. Elevated levels of PON1, by virtue of its potency to alleviate oxidative stress, could protect mice from suffering CCl<jats:sub>4<\/jats:sub>\u2010induced liver damage. Copyright \u00a9 2007 John Wiley &amp; Sons, Ltd.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jgm.1128","type":"journal-article","created":{"date-parts":[[2007,11,29]],"date-time":"2007-11-29T10:20:19Z","timestamp":1196331619000},"page":"94-100","source":"Crossref","is-referenced-by-count":20,"title":["Transgene expression of human PON1 Q in mice protected the liver against CCl<sub>4<\/sub>\u2010induced 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