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Study finds that IV venofer increases oxidative stress and immune modulation to increase M1 but decreased NK cell expression. The study found that this was related to the effects of the IV Fe2+ (ferrous) form; whereas the oral delivered Fe3+ (ferric) form. More free Fe2+ was released as a result of venofer infusion that was independent of transferrin. This was associated with increased oxidative stress.

The future of cancer therapy is cancer stem cells.  Study finds that Vitamin C, silymarin, and bee propolis blocks mitochondrial energy pathways in cancer stem cells.  Vitamin C is a known glycolytic inhbitor. Vitamin C was found to inhibit glycolysis via GAPDH targeting to inhibit the energy pathways of the mitochondria in CSCs.  The authors propse that Vitamin C can be used as add on therapies for conventional therapies to specifically attack the CSCs and their contribution to recrurence, treatment resistance, and metastasis potential all in addition to the ability of vitamin C to reduce the side effects of chemotherapy.

Good study shows that genetic polymorphisms play role in brain tumor risk with oxidative damage.  This study found an increased risk with SOD 2/3, and with CAT polymorphisms.  

Great diagram.  This diagram shows the current knowledge of how plaque is formed in arteries.  The major point here is the oxidation of LDL and the activation of the innate immune system and resultant inflammatory signaling.  In the vast majority of cases, the inflammation is driving this process, not the LDL.

Alpha lipoic acid is shown to protect the vascular endothelium against oxidative damage.

Pesticides disrupt the testicular function, in part, through oxidative damage.  This study found Alpha lipoic acid  to be a promising, effective mechanism to reduce the oxidative stress.  They also found tocopherols to be effect, but to a lesser extent.

T3 induces beneficial oxidative changes in muscles through its interaction with mitochondrial receptors.  PGC-1alpha and PPAR-gamma were involved in this process.  The important point here is that T3 is increasing oxidative function of muscle through interaction with mitochondria.

This study finds that T3 increases enzymes in the oxidative phosphorylation pathways and not in the glycolytic pathways in mitochondria.  This has enormous health implications, especially in cancer.  This also casts doubt on the current traditional medical dogma of hypothyroid evaluation and management which gives no regard to T3 in testing or therapy.

T3 in the post MI individual decreases the MI infarct size and the progression to heart failure. What is really  interesting about this study is that the T3 induced mitochondrial biogenesis and activity which is a great thing in recovery of MI and also in disease i.e. cancer.  However, it appears to increase HIF-1alpha and angiogenesis which is stimulated by retrograde signaling.  There is a muddied picture here.  Because T3 stimulates oxidative phosphorylation and mitochondria biogenesis which is favorable for health.  However, in this study of rats, it induced HIF-1alpha and angiogenesis in post MI, which is favorable to recovery, yet this is unfavorable for cancer.    Yet oxidative phosphorylation is favorable to cancer prevention/elimination and MI recovery.

oxidative stress decreased type 1 deiodinase activity and thus T4 to T3 conversion, resulting in increased rT3 production.  Of interesting note, Alpha lipoic acid increased type I deiodinase activity and T4 to T3 conversion.

animal study finds vitamin C improves hypertension via renovascular source and oxidative stress.  The dosage was 150 mg/kg/day.  This would be equivalent to 10,800 grams daily for a 72 human.  But what about a 200 lb male or female?  That would be 13,650 grams of vitamin C daily.

astaxanthin reduced oxidative stress biomarker and inflammation in human study.

glutathione redox reaction plays an important role in the ability to balance Th1 and Th2 and thus disease potential i.e. asthma as this study example.  

full study of previous abstract: low carb and high fat diet found to maintain muscle glycogen equal to high carb diet in endurance athletes.  Endurance athletes have high fat oxidation and this probably only applies to these endurance athletes; I would suspect this high fat oxidation would not be found in other short interval sports i.e. sprinting, football....

Omega 3 supplementation prevented oxidative stress in pregnancy.

CoQ10 supplementation of 150 mg in individuals with CAD found to have increased catalase activity, increased SOD activity, an increased MDA levels.  This reduced oxidative stress, TC, and LDL levels.

DASH diet shown to lower oxidative stress, inflammation, improve insulin resistance, lower inflammation, and aid weight loss.

LPS and minimal oxidized LDL have synergistic effects on inflammatory signaling.  Together the two promote inflammatory signaling from macrophages at much lower levels than either one alone.  They do this through macrophage NF-KappaB and AP-1 pathways.  And this resultant inflammation promotes atherosclerosis.  Where does all this start?  our diet and our gut.

Low physical activity and low TT in men associated with oxidized LDL.

Interesting study finds T4 therapy, levothyroxine,  linked to increased lung cancer.  The link could be through oxidative stress.