Protection mechanism of Se-containing protein hydrolysates from Se-enriched rice on Pb2+-induced apoptosis in PC12 and RAW264.7 cells

- SPHs protect cells against Pb2+-induced morphological changes of apoptosis.
- Caspase-dependent mitochondria pathway was potential protection mechanism of SPHs.
- Bcl-2 protein family and cytochrome C were involved in protection mechanism of SPHs.
- SPHs were low molecular weight Se peptides.

This study aimed to investigate the protection mechanism of Se-containing protein hydrolysates (SPH) from Se-enriched rice on Pb2+-induced apoptosis in PC12 and RAW264.7 cells. Results showed that SPHs could alleviate Pb2+-induced morphological changes of apoptosis and the loss of mitochondrial transmembrane potential in both cell types. Besides this, SPHs could significantly reduce the activation of caspase-3, -8, -9 induced by Pb2+, reverse the Pb2+-induced upregulation of Bax and release of cytochrome C, and downregulate Bcl-2 in cells. HPLC-ICP-MS and SEC-HPLC assays showed that SPHs were low molecular weight peptides (229.4-534.9 Da), and the major Se species found in SPHs was SeMet. Taken together, these findings suggested that SPHs could possibly protect the cells against Pb2+-induced apoptosis via a caspase-dependent mitochondrial pathway, and the primary effective constituents in SPHs were SeMet and Se-containing peptides, suggesting that SPHs might be a novel potential candidate to improve the health of people with Se deficiency or in Pb-contaminated areas.