ROS And Porphyria

Many people wonder what the link could possibly be between Porphyria and Multiple Chemical Sensitivity. For you obnoxious people who insist MCS is all in people heads without walking in their shoes we will term it "multiple allergy" for you. ROS is Reactive Oxygen Species and I won't explain that because it would take a whole lot of explaining and technical language. There has been no dispute that porphyrins do increase in MCS and no dispute that many with Porphyria have a hypersensitivity to many things including chemicals. I have had advocates on both sides blast me for trying to link the two. Honestly it's a shame these heads don't pull together to find out why instead of having tunnel vision.

A quote:
Fernando G. Princa, Adela Ana Juknata, Adrian A. Amitranoa and Alcira Batllea, ,



1. δ-Aminolevulinic acid (ALA) has been reported to promote reactive oxygen species (ROS). Overproduction and accumulation of ALA, as it occurs in acute intermittent porphyria (AIP), can be the origin of an endogenous source of ROS, which can then exert their oxidative damage to cell structures.

2. To investigate the induction of lipid peroxidation by ALA, thiobarbituric acid reactive substances and conjugated diene formation were measured by using minimal tissue units (MTUs) obtained from rat cerebellum. Malondialdehyde levels increased with ALA concentration and incubation time (72% at 1.0 mM ALA and 127% at 4.0 mM ALA for 4 hr), and conjugated diene formation was enhanced 50% in incubations with 1.0 mM ALA for 4 hr.

3. ALA-promoted ROS by exposure of cerebellum MTUs to 1.0 mM ALA during different intervals (1–4 hr) was partly reduced by the addition of antioxidants such as superoxide dismutase (SOD; 50 U/ml), catalase (4.5 μM) and dimethylsulfoxide (150 mM), demonstrating the involvement of O2−., H2O2 and OH. in ALA autooxidation.

4. Porphobilinogen biosynthesis was 170% increased when cerebellum MTUs were incubated with 1.0 mM ALA for 4 hr in the presence of SOD, suggesting that protein damage was promoted by ALA autooxidation.

5. These findings provide the first experimental evidence of the involvement of ALA-promoted ROS in the damage of proteins related to porphyrin biosynthesis, specially ALA-D. Oxidation of this enzyme would lead to further accumulation of ALA in AIP patients, which may be the origin of the well-known neuropsychiatric manifestations.


A link to the article http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T71-3VPJ5XB-1T&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=bdd6c2425f23565cd907dc811814a2a2

So what does this mean? ROS has been studied extensively in relation to MCS but I've never seen a study that showed how the porphyrin could accumulate. I have lots of theories on all of it and speak my mind quite a bit but every so often I find a study like this that actually backs it up. More on ROS later. So my next question is what would happen if one were to have the genetic form of Porphyria but a deficiency of glycine and/or folate such as in pregnancy? A little technical but maybe someone will look into it and provide an answer. I suspect a lower level of porphyrin in a 24hr urine test. And that leads me to a whole lot of other "what ifs".