PMID- 21540071 OWN - NLM STAT- MEDLINE DCOM- 20110926 LR - 20131121 IS - 1873-6351 (Electronic) IS - 0278-6915 (Linking) VI - 49 IP - 8 DP - 2011 Aug TI - In utero and lactational beta-carotene supplementation attenuates D-galactose-induced hearing loss in newborn rats. PG - 1697-704 LID - 10.1016/j.fct.2011.04.009 [doi] AB - D-Galactose could give rise to free radical damage by disturbing the some maternal antioxidants. The oxidative stress induced by D-galactose is a potent inducer of apoptosis, which is accompanied by the activation of protein-splitting enzymes called caspases. Apoptosis is a crucial physiological determinant of embryonic and neonatal development, and play an essential role in the development of the inner ear structures. Recently the increasing of D-galactose exposure is due to high consumption of dairy foods or reduced galactose metabolism. An overwhelming presence of D-galactose is known to become highly ototoxicity to humans. The purpose of this study was to investigate whether supplementation of pregnant and lactational mothers with beta-carotene could attenuate cochlear function damage and hair cells apoptosis induced by d-galactose in newborn rats. Pregnant rats were supplemented with D-galactose, or D-galactose and beta-carotene from gestational day (GD) 7 until postnatal day (PND) 21. On PND 22, offspring were examined in the distortion product otoacoustic emission (DPOAE) task, cochleae were then harvested for assessment of apoptosis by immunohistochemical stain for cysteine-aspartic acid proteases 3 (caspase-3) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. Maternal and offspring blood samples were then collected by direct cardiac puncture in heparin tubes, blood levels of D-galactose and beta-carotene were measured, plasma was separated for malondialdehyde (MDA) analysis, erythrocytes were left for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH). D-Galactose could significantly disturb the balance between maternal antioxidants and free radicals, and induce hearing loss in the offspring and cochlear hair cell apoptosis. In contrast, beta-carotene supplementation, coincidentally with D-galactose exposure, ameliorated these changes. Our data offer a conceptual framework for designing clinical trials using a safe micronutrient, beta-carotene, as a simple preventive strategy for D-galactose-induced ototoxicity. CI - Copyright (c) 2011 Elsevier Ltd. All rights reserved. FAU - Yu, Fei AU - Yu F AD - Department of Nutrition and Food Hygiene, School of Public Health, China Medical University, Heping District, Shenyang, Liaoning 110001, PR China. FAU - Hao, Shuai AU - Hao S FAU - Zhao, Yue AU - Zhao Y FAU - Yang, Hui AU - Yang H FAU - Fan, Xiao-Lan AU - Fan XL FAU - Yang, Jun AU - Yang J LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20110419 PL - England TA - Food Chem Toxicol JT - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JID - 8207483 RN - 0 (Antioxidants) RN - 0 (Caspase Inhibitors) RN - 01YAE03M7J (beta Carotene) RN - 4Y8F71G49Q (Malondialdehyde) RN - EC 1.11.1.9 (Glutathione Peroxidase) RN - EC 1.15.1.1 (Superoxide Dismutase) RN - EC 3.4.22.- (Casp3 protein, rat) RN - EC 3.4.22.- (Caspase 3) RN - GAN16C9B8O (Glutathione) RN - X2RN3Q8DNE (Galactose) SB - IM MH - Animals MH - Animals, Newborn MH - Animals, Suckling MH - Antioxidants/pharmacology MH - Apoptosis MH - Caspase 3/metabolism MH - Caspase Inhibitors MH - Dietary Supplements MH - Female MH - Galactose/*toxicity MH - Glutathione/blood MH - Glutathione Peroxidase/blood MH - Hearing Loss/*chemically induced/*drug therapy MH - Immunohistochemistry MH - In Situ Nick-End Labeling MH - Lactation MH - Lipid Peroxidation MH - Male MH - Malondialdehyde/blood MH - *Maternal Exposure MH - Oxidative Stress MH - Pregnancy MH - Rats MH - Rats, Wistar MH - Superoxide Dismutase/blood MH - beta Carotene/*pharmacology EDAT- 2011/05/05 06:00 MHDA- 2011/09/29 06:00 CRDT- 2011/05/05 06:00 PHST- 2010/09/21 00:00 [received] PHST- 2010/12/18 00:00 [revised] PHST- 2011/04/08 00:00 [accepted] PHST- 2011/05/05 06:00 [entrez] PHST- 2011/05/05 06:00 [pubmed] PHST- 2011/09/29 06:00 [medline] AID - S0278-6915(11)00145-1 [pii] AID - 10.1016/j.fct.2011.04.009 [doi] PST - ppublish SO - Food Chem Toxicol. 2011 Aug;49(8):1697-704. doi: 10.1016/j.fct.2011.04.009. Epub 2011 Apr 19.