Abstract #389
Section: Dairy Foods
Session: Dairy Foods III: Microbiology
Format: Oral
Day/Time: Tuesday 2:15 PM–2:30 PM
Location: 328
Session: Dairy Foods III: Microbiology
Format: Oral
Day/Time: Tuesday 2:15 PM–2:30 PM
Location: 328
# 389
Lactoferrin protect Caco-2, HEK, Hep-G2 and SK-N-SH cell lines inhibits aflatoxin-induced cytotoxicity and oxidative DNA damage.
H. Zhang1,4, N. Zheng1,2, J. Liu5, Y. N. Gao1,2, J. Q. Wang*1,2, 1Ministry of Agriculture-Key Laboratory of Quality & Safety Control for Milk and Dairy Products, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, China, 2Ministry of Agriculture-Laboratory of Quality and Safety Risk Assessment for Dairy Products, Beijing, China, 3Ministry of Agriculture-Milk and Dairy Product Inspection Center, Beijing, China, 4College of Food Science& Engineering, Ji Lin University, Chang Chun, China, 5China National Research Institute of Food and Fermentation Industries, Beijing, China.
Key Words: aflatoxin, lactoferrin, oxidative DNA damage
Lactoferrin protect Caco-2, HEK, Hep-G2 and SK-N-SH cell lines inhibits aflatoxin-induced cytotoxicity and oxidative DNA damage.
H. Zhang1,4, N. Zheng1,2, J. Liu5, Y. N. Gao1,2, J. Q. Wang*1,2, 1Ministry of Agriculture-Key Laboratory of Quality & Safety Control for Milk and Dairy Products, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, China, 2Ministry of Agriculture-Laboratory of Quality and Safety Risk Assessment for Dairy Products, Beijing, China, 3Ministry of Agriculture-Milk and Dairy Product Inspection Center, Beijing, China, 4College of Food Science& Engineering, Ji Lin University, Chang Chun, China, 5China National Research Institute of Food and Fermentation Industries, Beijing, China.
Aflatoxin is a natural potent carcinogen produced by Aspergillus flavus and A. parasiticus that can be detected in milk. It is a major cause of liver cancer. However, the involved molecular mechanisms and intervention methods remain largely unexplored. Lactoferrin (LF) was examined with regard to its potential role as a scavenger against radical oxygen. Moreover, no one has studied whether LF would inhibit the cytotoxicity of aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1). The purpose of this study was to evaluate the AFB1 and AFM1 induced cell toxicity by determining cell viability, membrane permeability and genotoxicity, and then investigate the capacity of LF to protect cells against AFB1 and AFM1. Cell viability, lactate dehydrogenase (LDH) release, TBARS and glutathione production and DNA damage were determined. In the Comet assay, DNA damage was quantified by assessing tail moment (TEM; arbitrary unit) and tail length (TL; arbitrary unit), as indicators of DNA strand breaks in single cell gel electrophoresis. Data showed that 4 µg/mL AFB1 or AFM1 could significantly inhibit Caco-2 cells, HEK cells, Hep-G2 cells, and SK-N-SH cell growth, increase lactate dehydrogenase (LDH) and cause genetic damage (P < 0.05). In comparison, AFB1 was found to be more toxic than AFM1 on all 4 cells especially on Hep-G2 cells, indicating liver is more sensitive than other organ as a an important detoxification system. All these cytotoxic outcomes might be associated with intracellular ROS generation, leading to membrane damage and DNA strand break. Significant reductions in cytotoxicity and oxidative DNA damage were observed when cells were pretreated with 10, 100 or 1000 µg/mL LF then exposed to 4 µg/mL AFB1 or AFM1. Our data suggested that AFB1 or AFM1 induces DNA damage in Caco-2 cells, HEK cells, Hep-G2 cells, and SK-N-SH cells, whereas that the antioxidant activity of LF may contribute to the alleviation of AFB1 or AFM1-induced cytotoxicity and DNA damage by reducing oxidative stress, it proved that LF plays an active role in inhibiting the toxicity of mycotoxins.
Key Words: aflatoxin, lactoferrin, oxidative DNA damage
