Kanchana Kengkoom1, Wannee Angkhasirisap1, Tapanee Kanjanapruthipong2, Rongdej Tungtrakanpoung3, Khwanchanok Tuentam3, Naphatson Phansom3, Sumate Ampawong4. 1. Academic Service Division, National Laboratory Animal Center, Mahidol University, 999, Salaya, Puttamonthon, Nakorn Pathom, 73170, Thailand. 2. Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6, Ratchawithi Road, Ratchathewi, Bangkok, 10400, Thailand. 3. Department of Biology, Faculty of Science, Naresuan University, 99, Moo 9, Phitsanulok-NakornSawan Road, Phitsanulok, 65000, Thailand. 4. Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6, Ratchawithi Road, Ratchathewi, Bangkok, 10400, Thailand. am_sumate@hotmail.com.
Abstract
BACKGROUND: Alpha-2u globulin nephropathy mainly shows toxicological pathology only in male rats induced by certain chemicals and drugs, such as levamisole (antiparasitic and anticancer drugs). Streptozotocin (STZ) is also an anticancer-antibiotic agent that has been used for decades to induce a diabetic kidney disease model in rodents. The purpose of this study is to determine if STZ causes alpha-2u globulin nephropathy in male rats during an advanced stage of diabetic kidney disease. Alpha-2u globulin nephropathy, water absorption and filtration capacities (via aquaporin [AQP]-1, - 2, - 4 and - 5) and mitochondrial function (through haloacid dehalogenase-like hydrolase domain-containing protein [HDHD]-3 and NADH-ubiquinone oxidoreductase 75 kDa subunit [NDUFS]-1 proteins) were examined in STZ-induced diabetic Wistar rat model. RESULTS: More than 80% of severe clinical illness rats induced by STZ injection simultaneously exhibited alpha-2u globulin nephropathy with mitochondrial degeneration and filtration apparatus especially pedicels impairment. They also showed significantly upregulated AQP-1, - 2, - 4 and - 5, HDHD-3 and NDUFS-1 compared with those of the rats without alpha-2u globulin nephropathy. CONCLUSIONS: STZ-induced alpha-2u globulin nephropathy during diabetic kidney disease in association with deterioration of pedicels, renal tubular damage with adaptation and mitochondrial driven apoptosis.
BACKGROUND:Alpha-2u globulinnephropathy mainly shows toxicological pathology only in male rats induced by certain chemicals and drugs, such as levamisole (antiparasitic and anticancer drugs). Streptozotocin (STZ) is also an anticancer-antibiotic agent that has been used for decades to induce a diabetic kidney disease model in rodents. The purpose of this study is to determine ifSTZ causes alpha-2u globulinnephropathy in male rats during an advanced stage of diabetic kidney disease. Alpha-2u globulinnephropathy, water absorption and filtration capacities (via aquaporin [AQP]-1, - 2, - 4 and - 5) and mitochondrial function (through haloacid dehalogenase-like hydrolase domain-containing protein [HDHD]-3 and NADH-ubiquinone oxidoreductase 75 kDa subunit [NDUFS]-1 proteins) were examined in STZ-induced diabetic Wistarrat model. RESULTS: More than 80% of severe clinical illness rats induced by STZ injection simultaneously exhibited alpha-2u globulinnephropathy with mitochondrial degeneration and filtration apparatus especially pedicels impairment. They also showed significantly upregulated AQP-1, - 2, - 4 and - 5, HDHD-3 and NDUFS-1 compared with those of the rats without alpha-2u globulinnephropathy. CONCLUSIONS:STZ-induced alpha-2u globulinnephropathy during diabetic kidney disease in association with deterioration of pedicels, renal tubular damage with adaptation and mitochondrial driven apoptosis.
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Authors: Luigi Rossi; Maria Celeste Nicoletti; Monica Carmosino; Lisa Mastrofrancesco; Antonella Di Franco; Francesca Indrio; Rossella Lella; Luigi Laviola; Francesco Giorgino; Maria Svelto; Loreto Gesualdo; Giuseppe Procino Journal: J Diabetes Res Date: 2017-01-26 Impact factor: 4.011