2. Academic Validation
  3. Cytotoxicity of adducts formed between quercetin and methylglyoxal in PC-12 cells

Cytotoxicity of adducts formed between quercetin and methylglyoxal in PC-12 cells

  • Food Chem. 2021 Aug 1:352:129424. doi: 10.1016/j.foodchem.2021.129424.
Pengzhan Liu 1,  Zhao Yin 2,  Min Chen 3,  Caihuan Huang 3,  Zhihui Wu 4,  Junqing Huang 5,  Shiyi Ou 3,  Jie Zheng 6
Affiliations

Affiliations

  • 1 School of Food Science and Engineering, South China University of Technology, Guangzhou, Guangdong 510641, China.
  • 2 Department of Hematology, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong 510317, China; School of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, China.
  • 3 Department of Food Science and Engineering, Jinan University, Guangzhou 510632, China.
  • 4 Department of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou 510632, China.
  • 5 Formula-pattern Research Center, School of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
  • 6 Department of Food Science and Engineering, Jinan University, Guangzhou 510632, China. Electronic address: [email protected].
PMID: 33706136 DOI: 10.1016/j.foodchem.2021.129424
Abstract

Quercetin (Que) or quercetin-containing food stuffs are widely incorporated in bakery foods for improving food texture and health effects, and scavenging reactive aldehydes, such as methylglyoxal (MGO) that exhibits various deleterious effects including contribution to neurodegeneration. This study aimed to investigate the cytotoxicity of the adducts formed between quercetin and MGO resulted from the incorporation of quercetin in foods. Two highly-purified adducts (Que-mono-MGO and Que-di-MGO) were found to display higher cytotoxicity than their precursor MGO and quercetin. They elevated Apoptosis via upregulation of expression of apoptotic markers, including p-P38, cleaved caspase-9 and -3, and pro-apoptotic Bax. They induced mitochondrial dysfunction via decreasing mitochondrial membrane potential and increasing Lactate Dehydrogenase release. Moreover, they attenuated levels of p-Akt, Nrf2, NQO-1, and HO-1, proving that they induced neurodegeneration Apoptosis through mitochondria-mediated signaling pathways (PI3K-Akt and Nrf2-HO-1/NQO-1). These findings indicated that the safety consequence of MGO after scavenged by Polyphenols needs to be concerned.

Keywords

AKT/Nrf2 signaling pathway; Cookies; Mitochondria-mediated apoptosis; Mitochondrial dysfunction; Neurotoxicity; Quercetin-methylglyoxal adduct.

Figures
Products