The neuronal protection of a zinc-binding protein isolated from oyster

Wei Hsuan Hsu, Yu Chun Lin, Bo Rui Chen, She Ching Wu, Bao Hong Lee

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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 of D-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 of D-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 by D-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.

Original languageEnglish
Pages (from-to)61-68
Number of pages8
JournalFood and Chemical Toxicology
Volume114
DOIs
Publication statusPublished - 2018 Apr

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All Science Journal Classification (ASJC) codes

  • Food Science
  • Toxicology

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