Here's another article [Preusch and Suttie, 1981: (http://jn.nutrition.org/cgi/reprint/111/12/2087.pdf) (http://www.ncbi.nlm.nih.gov/pubmed/7310534)] that shows that riboflavin (vitamin B2) can enhance clotting factor production by activating either DT-diaphorase (NQO1) or a "warfarin-insensitive" enzyme that can help in the regeneration of vitamin K. One could say that this is secondary to an increase in the availability of reducing equivalents or something or that riboflavin is enhancing respiratory chain activity. I don't think that's what's happening, though, because these are cytosolic or plasma-membrane enzymes they're talking about. They're not mitochondrial enzymes. There are strange things about the timecourse of riboflavin-induced changes, also, and the researchers don't understand the mechanism completely. Researchers have discussed this kind (I say kind because it's not clear if this is one enzyme or multiple enzymes with similar and potentially-broad substrate specificities, etc.) of enzyme as being responsible for the cytosolic or even the plasma membrane reduction and "regeneration" of coenzyme Q10 [Turunen et al., 2004: (http://www.ncbi.nlm.nih.gov/pubmed/14757233)]. The idea has been that this could explain coenzyme Q10's supposed "respiratory-chain-enhancement-independent" antioxidant activities, but this plasma membrane quinone reductase has NAD(P)H oxidase activity (Turunen et al., 2004). That suggests that coenzyme Q10 could basically increase the activity of this quinone reductase (or other reductases), increase clotting factor production, in theory, as riboflavin has been shown to (Preusch and Suttie, 1981), and also produce reactive oxygen species by that mechanism.
The mechanisms by which riboflavin and coenzyme Q10 could augment the vitamin K cycle are not very clear, even though that article by Preusch and Suttie (1981) is very clearly-written and sheds a lot of light on the issue. Gage and Milligan (2005) [Brian Gage and Paul Milligan, 2005: (http://www.ncbi.nlm.nih.gov/pubmed/16043212)] suggested that coenzyme Q10 may have vitamin K activity, and I discussed some of the issues previously [(http://hardcorephysiologyfun.blogspot.com/2009/01/different-perspectives-on-coq10-and.html); (http://hardcorephysiologyfun.blogspot.com/2009/01/vitamin-k-activity-and-coq10-concerns.html); (http://hardcorephysiologyfun.blogspot.com/2009/01/reference-on-old-practice-of-using.html)]. Both the classical enzymes of the vitamin K cycle and these nonclassical enzymes essentially recycle small amounts of vitamin K (and keep cycling it through the enzymes in sequential oxidation-reduction reactions) for use in the post-translational maturation (gamma-carboxylation) of clotting factor proteins (vitamin K is not a clotting factor, but it's used to produce clotting factors). Riboflavin and coenzyme Q10 have both been used for many of the same purposes in some people with mitochondrial disorders, to enhance complex I activity [Scholte et al., 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7599230); Bernsen et al., 1993: (http://www.ncbi.nlm.nih.gov/pubmed/8229067); Triepels et al., 2001: (http://www.ncbi.nlm.nih.gov/pubmed/11579423)], and this could suggest that either riboflavin or coenzyme Q10 could act by just enhancing the recycling of the vitamin K pool. But I'm not so sure. Some strange compounds have vitamin K activity, and it's possible riboflavin has some kind of crazy ability to substitute for vitamin K. Some pyridine-based drugs or pyrimidine-based drugs can have vitamin K activity, and a lot about vitamin K, in relation to warfarin, is not understood well. This all depends on what one means by "vitamin K activity," and another issue is the extent to which superfluous riboflavin or coenzyme Q10 would enhance the vitamin K cycle. Preusch and Suttie (1981) discuss the effects of riboflavin in terms of deficiency or sufficiency, but I'm not sure that's the issue. This research suggests to me that excesses of riboflavin or coenzyme Q10 could keep enhancing, up to a point, the activities of these enzymes. This would raise concerns, in my mind, about the use of the whole "high-dose riboflavin" thing in the treatment of migraines. Riboflavin and CoQ10 have both been used to treat migraines, and the idea is that they both work by enhancing the activities of respiratory-chain enzymes (enhancing complex I and II activities, basically). But in people with thrombogenic tendencies, these articles suggest that there could be cause for concern about the use of CoQ10 or riboflavin.
Riboflavin-derived coenzymes (FMN and FAD) have actually been shown, in other articles, to enhance the activities of enzymes of the vitamin K cycle [Wosilait, 1960: (http://www.jbc.org/cgi/reprint/235/4/1196) (http://www.ncbi.nlm.nih.gov/pubmed/13846011)]. Wosilait (1960) also showed that coenzyme Q10 could serve as a substitute electron acceptor in one of those reactions by a vitamin K-cycle enzyme. This article [Ross, 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15554240)] discusses the different capacities of NQO1 and NQO2, quinone oxidoreductase enzymes that use riboflavin-derived coenzymes as cofactors (they're "flavoenzymes"), to act as vitamin K reductases, to regenerate coenzyme Q10, and to produce reactive oxygen species en masse. There's actually some research showing that methylenetetrahydrofolate reductase (CH2THFR), a riboflavin-derived-coenzyme-dependent enzyme, can act as a menadione (vitamin K3) reductase [Vanoni et al., 1983: (http://www.jbc.org/cgi/reprint/258/19/11510.pdf) (http://www.ncbi.nlm.nih.gov/pubmed/6352699)]. But, again, riboflavin would be expected to enhance the activity of that. The folates could conceivably synergize with riboflavin in that regard, and I remember one article discussing the capacity of some folates to act as electron acceptors. But folates have never been shown to have the kinds of "redox properties" that riboflavin and coenzyme Q10 have. It would be something to keep in mind, though, at high doses of folates. But folates are more substrates than electron acceptors for reductase enzymes, and folates have never been used as standalone treatments to treat mitochondrial disorders. Nonetheless, riboflavin has been used to enhance CH2THFR activity and to reduce homocysteine a little, and it might be wise for people with blood vessel disease to not use high doses of riboflavin. There's no point in being afraid of riboflavin, because it's essential. But it's worthwhile to be aware of the range and dose-dependencies of the effects of these things. Although it's a crude argument, it's helpful to sometimes look at the absolute amounts of these things. Riboflavin is being used in dosages of 50-400 mg/d for these supposedly therapeutic purposes, and reduced folates have generally been used in dosages ranging from 15-30 mg/d (two studies have used either 50 or 90 mg/d of methylfolate). Obviously there's the issue of how much gets into the cells, but I think there could be a dose-dependency to these effects on the vitamin K cycle.
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