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We determined that ethanol exposure induced a reversible, time-dependent, saturable increase in functional peroxisomes labeled with either marker. This increase was due to ethanol-induced oxidative stress. In cells treated with oleic acid (to mimic fatty liver), only ABCD3-positive peroxisomes proliferated, and preferentially colocalized with lipid droplets in cells treated with oleic acid alone and\/or with ethanol. In cells overexpressing the tubulin-specific acetyltransferase, \u03b1TAT1, we determined that peroxisome-lipid droplet contacts were mediated by acetylated microtubules. Peroxisome proliferation was also observed in ethanol-fed mouse and rat livers, but was absent in fibrotic mouse models of liver injury and in samples from individuals with alcohol-induced cirrhosis suggesting that alcohol exposure promotes an early hepatoprotective rise in peroxisomes that is lost as the condition progresses to fibrosis. Our studies further suggest that peroxisome proliferator-activated receptor agonists may be an effective intervention for early ethanol-associated liver disease. <\/jats:p>","DOI":"10.1091\/mbc.e24-06-0252","type":"journal-article","created":{"date-parts":[[2024,11,13]],"date-time":"2024-11-13T16:54:17Z","timestamp":1731516857000},"source":"Crossref","is-referenced-by-count":6,"title":["Distinct peroxisome populations differentially respond to alcohol-associated hepatic injury"],"prefix":"10.1091","volume":"35","author":[{"given":"Ramyajit","family":"Mitra","sequence":"first","affiliation":[{"name":"Department of Biology, The Catholic University of America, Washington, DC, 20064"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raghabendra","family":"Adhikari","sequence":"additional","affiliation":[{"name":"Department of Biology, The Catholic University of America, Washington, DC, 20064"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saniya 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