Inhibition of apoptosis by menadione on exposure to UVA

Abstract

Quinones are widely distributed in the environment, both as natural products and as pollutants. This paper reports that one of the simplest quinones, 2-methyl-1,4-naphthoquinone (menadione), effectively inhibited apoptosis in the presence of UVA. Menadione suppressed the apoptosis induced by serum depletion and cell detachment. This effect was significantly enhanced by UVA irradiation. An antioxidant, N-acetylcysteine, completely inhibited the antiapoptotic effects of both menadione itself and menadione plus UVA, and peroxidation of the cells after treatment was observed using a probe to detect the intracellular production of peroxides. By contrast, 2-hydroxy-1,4-naphtoquinone (lawsone) showed no antiapoptotic effect in the presence or absence of UVA. Lawsone is reported not to undergo the redox process that produces reactive oxygen species. These results indicated that intracellular peroxidation contributed to the antiapoptotic effects of both menadione itself and menadione plus UVA. Dysregulation of the apoptotic process is critical to carcinogenesis. The photosensitization of quinone compounds as it relates to the inhibition of apoptosis should be examined in the future.

Antiproliferative and apoptotic effects of spanish honeys

“…Moreover, alterations in the redox status of the cell to a more oxidizing environment occurs prior to the final phase of caspase activation in many model of apoptosis. [13] Recent results showed honey as a plausible candidate for induction of apoptosis through ROS and mitochondria-dependent mechanism in colon cancer cells. [14] In addition, since the composition of honey varies widely in relation to its botanical origin and environmental factors, it can be reasonably expected that honey properties from different floral sources are different.…”

Antiapoptotic effects of dietary antioxidants towards N‐nitrosopiperidine and N‐nitrosodibutylamine‐induced apoptosis in HL‐60 and HepG2 cells

“…Many studies have supported the hypothesis that apoptosis can be initiated by oxidative stress, which in turn is mediated by the generation of reactive oxygen species (ROS) (Buttke and Sandstrom, 1994;Ibuki et al, 2006). ROS may act as signaling molecules for the initiation and the execution of apoptosis (Carmody and Cotter, 2001).…”

Near-UV Photolysis of 2-Methyl-1,4-naphthoquinone−DNA Duplexes: Characterization of Reversible and Stable Interstrand Cross-Links between Quinone and Adenine Moieties

“…The mechanism of toxicity for MQ is not entirely clear. On the one hand, MQ promoted apoptosis in cells via its redox cycling properties (14), whereas on the other hand, it inhibited apoptosis following near-UV photolysis (15). Three mechanisms of action have been proposed to account for the action of MQ in cell culture: (1) the generation of reactive oxygen species by quinone redox cycling and type II photosensitization (16); (2) the conjugation of MQ with the thiol groups of proteins, leading to the depletion of glutathione and changes in intracellular [Ca 2+ ] (17,18); and (3) the direct activation of transcription factors and other proteins by arylation with MQ (19).…”