The neuronal protection of a zinc-binding protein isolated from oyster. (April 2018)

• Record Type: Journal Article
• Authors: Hsu, Wei-Hsuan; Lin, Yu-Chun; Chen, Bo-Rui; Wu, She-Ching; Lee, Bao-Hong
• Is Part Of: Food and chemical toxicology. Volume 114(2018)
• Page Start: 61
• Page End: 68
• Publication Date: 2018-04
• Subjects: Oxidative stress -- Metallothionein-3 (MT-3) -- d-galactose -- Zinc-binding protein of oyster -- Amyloid beta (Aβ); Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2018.02.009
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: Mitochondrial function is applied as oxidative stress and neuronal damage index. In this study, d -galactose was used to induce free radicals production and neuronal damage in HN-h cells, and the effect of novel 43 kDa protein isolated from oyster on anti-mitochondrial dysfunction and zinc-binding ability were evaluated. Crystal violet stain results indicated zinc-binding protein of oyster (ZPO) attenuated neuronal cell death induced by 100 mM ofd -galactose on HN-h cells in a dose-dependent manner. ZPO alleviated mitochondrial inactivation, mitochondrial membrane potential decreasing, oxidative stress, and fusion/fission state in non-cytotoxic concentration ofd -galactose (50 mM)-treated HN-h cells. ZPO treatment recovered metallathionein-3 (MT-3) decrease and inhibited β- and γ-secretase as well as amyloid beta (Aβ) accumulation in HN-h cells caused byd -galactose induction. These results suggest ZPO could avoid oxidative stress and is a functional protein for zinc concentration maintainability, which has potential for development of functional foods for neuronal protection. Highlights: Protein isolates from oyster (ZPO) has zinc binding ability. ZPO attenuated mitochondrial dysfunction. ZPO protects neurons against oxidative stress. ZPO inhibited Aβ accumulation in neuron cells. ZPO has potential as pharmaceutical protein.