{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:41:36Z","timestamp":1792708896806,"version":"4.5.0"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2011,12,22]],"date-time":"2011-12-22T00:00:00Z","timestamp":1324512000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mercury is an environmental toxicant that can disrupt brain development. However, although progress has been made in defining its neurotoxic effects, we know far less about available therapies that can effectively protect the brain in exposed individuals. We previously developed an animal model in which we defined the sequence of events underlying neurotoxicity: Methylmercury (MeHg) injection in postnatal rat acutely induced inhibition of mitosis and stimulated apoptosis in the hippocampus, which later resulted in intermediate\u2010term deficits in structure size and cell number. N\u2010acetyl cysteine (NAC) is the N\u2010acetyl derivative of L\u2010cysteine used clinically for treatment of drug intoxication. Here, based on its known efficacy in promoting MeHg urinary excretion, we evaluated NAC for protective effects in the developing brain. In immature neurons and precursors, MeHg (3 \u03bcM) induced a &gt;50% decrease in DNA synthesis at 24 hr, an effect that was completely blocked by NAC coincubation. In vivo, injection of MeHg (5 \u03bcg\/g bw) into 7\u2010day\u2010old rats induced a 22% decrease in DNA synthesis in whole hippocampus and a fourfold increase in activated caspase\u20103\u2010immunoreactive cells at 24 hr and reduced total cell numbers by 13% at 3 weeks. Treatment of MeHg\u2010exposed rats with repeated injections of NAC abolished MeHg toxicity. NAC prevented the reduction in DNA synthesis and the marked increase in caspase\u20103 immunoreactivity. Moreover, the intermediate\u2010term decrease in hippocampal cell number provoked by MeHg was fully blocked by NAC. Altogether these results suggest that MeHg toxicity in the perinatal brain can be ameliorated by using NAC, opening potential avenues for therapeutic intervention. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22819","type":"journal-article","created":{"date-parts":[[2011,12,23]],"date-time":"2011-12-23T04:47:41Z","timestamp":1324615661000},"page":"743-750","source":"Crossref","is-referenced-by-count":43,"title":["N\u2010acetyl cysteine treatment reduces mercury\u2010induced neurotoxicity in the developing rat 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