Comparison of the effects of an organic and an inorganic form of selenium on a mammary carcinoma cell line

Abstract

The development of new compounds with greater cancer inhibitory activity and that are well tolerated continues to be a priority in chemoprevention research involving selenium. One compound, 1,-4-phenylene-bis(methylene)selenocyanate (p-XSC), is representative of a series of organoselenium compounds with these characteristics. In this study, the effects of p-XSC on a mouse mammary carcinoma cell line were compared to those of sodium selenite, which has been shown to be growth inhibitory. Treatment with p-XSC caused a 3- to 6-fold greater accumulation of selenium within cells than did treatment with equivalent amounts of selenite and cells were able to better tolerate higher cellular levels of selenium derived from p-XSC. Both compounds resulted in a dose-dependent reduction in cell number after 24 h of exposure. Selenite and p-XSC also caused a dose-dependent increase in cell death by apoptosis. This effect was observed within 5 h of treatment. The effect of p-XSC on apoptosis was more pronounced than that of selenite, especially at the 20 microM level of exposure. The induction of apoptosis by selenium compounds may partially account for their chemopreventive activity.

The JNK signaling pathway is involved in sodium-selenite-induced apoptosis mediated by reactive oxygen in HepG2 cells

“…Many studies have showed that the inhibition effect of the growth of cancer cells may indicate that Se plays an important role in exerting carcinostatic activity. 17,[29][30][31][32] Our study further shows that such an inhibition effect is dose-and timedependent. The growth of HepG2 cells was inhibited when they were exposed to Selenite (>5 μM) for more than 24 h or to Selenite (>10 μM) for more than 12 h.…”

Whole blood selenium levels (WBSL) in patients with prostate cancer (PC), benign prostatic hyperplasia (BPH) and healthy male inhabitants (HMI) and prostatic tissue selenium levels (PTSL) in patients with PC and BPH

“…The way in which selenium could suppress neoplasia is not clear at all. In vitro, selenium compounds produce direct anti-tumour effects, as demonstrated by tumour cell growth inhibition and apoptosis promotion [32]. A large portion of selenium is incorporated into glutathione peroxidase, which is known to reduce lipid peroxide.…”

Selen und seine anorganischen Verbindungen [MAK Value Documentation in German language, 1999]

“…Selenodiglutathion induziert DNA-Fragmente Wu et al 1995), die als charakteristisches Zeichen für Apoptose angesehen werden (Bicknell et al 1994;Oberhammer et al 1993). Die Induktion von Apoptose wurde für Selenit und Selenodiglutathion nachgewiesen (Forrest et al 1994;Lanfear et al 1994;Thompson et al 1994). In verschiedenen Zellinien wirkten Selenodiglutathion (Poirier und Milner 1983;Santoro und Milner 1991) � Natriumselenit (Medina und Oborn 1984;Thompson et al 1994) � Dimethylselenid (Poirier und Milner 1983) � Selenocystein (Batist et al 1986) nicht aber Selenat oder Selenomethionin (Yan et al 1991) wachstumshemmend.…”