FOOD SCIENCE ›› 2018, Vol. 39 ›› Issue (1): 136-141.doi: 10.7506/spkx1002-6630-201801021

• Nutrition & Hygiene • Previous Articles     Next Articles

Water-Soluble Advanced Glycation End Products from Bread Crust Cause Oxidative Damage to Human Kidney Tubular Epithelial Cells

JIA Benpan, YUAN Xiaojin, FAN Zhiyi, HU Jing, LI Juxiu*   

  1. College of Food Science and Engineering, Northwest A & F University, Yangling 712100, China
  • Online:2018-01-15 Published:2018-01-05

Abstract: Advanced glycation end products (AGEs) are a class of compounds that are formed during thermal processing and storage of foods, which are significantly associated with various chronic diseases, such as cardiovascular diseases, diabetes, and kidney diseases. In the present study, bread crust extract (BCE), rich in AGEs, was obtained from bread crust through water extraction, and we investigated if BCE could cause intracellular oxidative stress and cell damage in human kidney tubular epithelial cells (HKCs). HKCs were treated with different BCE concentrations for determining the appropriate concentration of BCE by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay for use in subsequent experiments. The effect of BCE on intracellular oxidative stress balance and the degree of cell damage was evaluated by detecting the levels of intracellular reactive oxygen species (ROS), total superoxide dismutase (SOD) and malondialdehyde (MDA) and lactic dehydrogenase (LDH) in supernatants. The results indicated that the level of ROS in HKCs was increased along with increasing BCE concentration after being cultured with different concentrations of BCE for 24 h, and reached a maximum value at 8 and 12 mg/mL. Intracellular MDA contents increased significantly at 4 and 8 mg/mL of BCE (P < 0.01), but markedly declined at 12 mg/mL (P < 0.05). On the contrary, intracellular SOD activity was reduced with increasing concentration of BCE, and significantly decreased at BCE concentrations of 8 and 12 mg/mL. The level of secreted LDH was increased with increasing BCE concentrations, and the increase was highly significant at 8 and 12 mg/mL (P < 0.01). Therefore, BCE can cause serious damage to HKCs via elevating intracellular ROS levels, inhibiting total SOD activity and thereby promoting lipid peroxidation reaction, altering the cell membrane permeability, and consequently improving extracellular LDH activity.

Key words: human kidney tubular epithelial cells, bread crust extract, oxidative damage, lipid peroxidation

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