Green synthesized selenium nanoparticle as carrier and potent delivering agent of s-allyl glutathione: Anticancer effect against hepatocarcinoma cell line (HepG2) through induction of cell cycle arrest and apoptosis

• Published in: Journal of drug delivery science and technology Vol. 53; p. 101207
• Main Authors: Krishnan, Vennila, Loganathan, Chitra, Thayumanavan, Palvannan
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.10.2019
• Subjects: Apoptosis; DNA fragmentation; Endogenous antioxidants; Hepatocellular carcinoma; Oxidative stress; S-allyl glutathione; Selenium nanoparticles; Oxidative stress; DNA fragmentation; Endogenous antioxidants; S-allyl glutathione; Hepatocellular carcinoma; Selenium nanoparticles; Apoptosis
• ISSN: 1773-2247
• DOI: 10.1016/j.jddst.2019.101207

S-allyl glutathione (SAG) is an analog of glutathione (GSH) synthesized by alkalating the thiol group of GSH with the allyl group. Previously, SAG has shown potent topoisomerase inhibition in in vitro, an important target protein of cancer treatment. Hence, in the present study SAG conjugated selenium nanoparticles was synthesized using Spermacoce hispida aqueous leaf extract (SAG-Sh-SeNPs). SAG was released from SAG-Sh-SeNPs equivalently in the buffer with various pH such as 5.3 (acidic) and 7.4 (close to neutral). SAG-Sh-SeNPs was investigated for anticancer potential against hepatocarcinoma cell line (HepG2). SAG-Sh-SeNPs treatment increased reactive oxidant species level in HepG2 which was inhibited by GSH pretreatment. Also, SAG-Sh-SeNPs treatment decreased the endogenous antioxidants level such as GSH, superoxide dismutase, catalase and GSH peroxidase. In addition, SAG-Sh-SeNPs disrupted the mitochondrial membrane potential and initiated DNA fragmentation. Altogether, the SAG-Sh-SeNPs treatment induced cell cycle arrest at sub-G1 phase and further lead to apoptosis which was visualized by acridine orange/ethidium bromide staining. [Display omitted]