Mitochondrial Peptide Humanin Protects Silver Nanoparticles-Induced Neurotoxicity in Human Neuroblastoma Cancer Cells (SH-SY5Y).
Gurunathan. Sangiliyandi S; Jeyaraj. Muniyandi M; Kang. Min-Hee MH; Kim. Jin-Hoi JH
Key Findings
- Silver nanoparticles (≈18 nm) damage SH‑SY5Y neuroblastoma cells by causing oxidative stress, loss of mitochondrial membrane potential, ATP depletion, and apoptosis
- Humanin pretreatment or co‑treatment markedly reduces these toxic effects, preserving cell viability and mitochondrial function
- This is the first report that humanin can protect neural cells from nanoparticle‑induced neurotoxicity
Practical Outcomes
- Humanin shows promise as a neuroprotective agent against oxidative stress, but the work is limited to cell cultures and uses silver nanoparticles, which aren’t a common exposure for most people. No dosing guidelines or human data are available, so biohackers should view this as early‑stage evidence rather than a ready‑to‑use supplement protocol.
Summary
The study shows that the tiny protein humanin can shield brain‑derived cells from damage caused by silver nanoparticles, which are known to create oxidative stress and kill cells. In lab dishes, giving cells humanin before or together with the nanoparticles helped keep the cells alive, maintained their energy factories, and reduced DNA damage and cell death.
Abstract
The extensive usage of silver nanoparticles (AgNPs) as medical products such as antimicrobial and anticancer agents has raised concerns about their harmful effects on human beings. AgNPs can potentially induce oxidative stress and apoptosis in cells. However, humanin (HN) is a small secreted peptide that has cytoprotective and neuroprotective cellular effects. The aim of this study was to assess the harmful effects of AgNPs on human neuroblastoma SH-SY5Y cells and also to investigate the protective effect of HN from AgNPs-induced cell death, mitochondrial dysfunctions, DNA damage, and apoptosis. AgNPs were prepared with an average size of 18 nm diameter to study their interaction with SH-SY5Y cells. AgNPs caused a dose-dependent decrease of cell viability and proliferation, induced loss of plasma-membrane integrity, oxidative stress, loss of mitochondrial membrane potential (MMP), and loss of ATP content, amongst other effects. Pretreatment or co-treatment of HN with AgNPs protected cells from several of these AgNPs induced adverse effects. Thus, this study demonstrated for the first time that HN protected neuroblastoma cells against AgNPs-induced neurotoxicity. The mechanisms of the HN-mediated protective effect on neuroblastoma cells may provide further insights for the development of novel therapeutic agents against neurodegenerative diseases.
Study Information
pubmed
2019
2019-09-09T00:00:00.000Z
10.3390/ijms20184439
36
125