{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:19:37Z","timestamp":1792801177381,"version":"4.5.0"},"reference-count":74,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2024,8,13]],"date-time":"2024-08-13T00:00:00Z","timestamp":1723507200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Toxicol Ind Health"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:p>\n                    Aluminium, a ubiquitous environmental toxicant, is distinguished for eliciting a broad range of physiological, biochemical, and behavioural alterations in laboratory animals and humans. The present work was conducted to study the functional and structural changes induced by aluminium in rat liver. Twenty five adult male Wistar rats (150\u2013200 g) were randomly divided into five groups; control group and four Al-treated groups viz: Al 1 (25\u00a0mg AlCl\n                    <jats:sub>3<\/jats:sub>\n                    \/kg b.wt), Al 2 (35\u00a0mg AlCl\n                    <jats:sub>3<\/jats:sub>\n                    \/kg b.wt), Al 3 (45\u00a0mg AlCl\n                    <jats:sub>3<\/jats:sub>\n                    \/kg b.wt), and Al 4 (55\u00a0mg AlCl\n                    <jats:sub>3<\/jats:sub>\n                    \/kg b.wt). Rats in the aluminium-treated groups were administered AlCl\n                    <jats:sub>3<\/jats:sub>\n                    for 30 days through oral gavage. Aluminium significantly increased the serum levels of liver function markers (ALT, AST, and ALP), phospholipids, and cholesterol. The activities of hepatocyte membrane (ALP, GGT, and LAP) and carbohydrate metabolic (G6P, F16BP, HK, LDH, MDH, ME, and G6PDH) enzymes were significantly altered by AlCl\n                    <jats:sub>3<\/jats:sub>\n                    administration. Prolonged Al exposure induced oxidative stress in the liver, as evident by significant hepatocellular DNA damage, increased lipid peroxidation, and decreased non-enzymatic and enzymatic antioxidants. The toxic effects observed in this study were AlCl\n                    <jats:sub>3<\/jats:sub>\n                    dose-dependent. Histopathological examination of liver sections revealed enlargement of sinusoidal spaces, derangement of the hepatic chord, loss of discrete hepatic cell boundaries, congestion of hepatic sinusoids, and degeneration of hepatocytes in Al-intoxicated rats. In conclusion, aluminium causes severe hepatotoxicity by inhibiting the hepatocyte membrane enzymes and disrupting the liver\u2019s energy metabolism and antioxidant defence.\n                  <\/jats:p>","DOI":"10.1177\/07482337241269784","type":"journal-article","created":{"date-parts":[[2024,8,14]],"date-time":"2024-08-14T01:22:00Z","timestamp":1723598520000},"page":"581-595","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":5,"title":["Chronic aluminium chloride exposure induces redox imbalance, metabolic distress, DNA damage, and histopathologic alterations in Wistar rat liver"],"prefix":"10.1177","volume":"40","author":[{"given":"Farha","family":"Shahabuddin","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh, 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