And the progestin phases have an activation phase; the proliferation phase involves an increase in the production and consumption of energy, which continuesCornelli et al. Reproductive Biology and Endocrinology 2013, 11:74 http://www.rbej.com/content/11/1/Page 4 ofTable 2 d-ROMs test, E2, P4 values at various times in healthy volunteers (average ?SD)t1 d-ROMs CARR.U. 284 +/- 38.0 E2 pg/mL t3 273 +/- 47.0 t6 284 +/- 34.6 99 +/- 33.7 P4 ng/mL t9 299a +/- 31.3 222b +/- 34.2 t12 336a +/- 66.8 195b +/- 39.9 1.7 +/- 0.at15 378a +/- 115.6 134b +/- 36.t18 326a +/- 66.4 157b PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 +/- 36.9 6.3c +/- 3.t21 315a +/- 56.3 126 +/- 38.4 13.0c +/- 6.t24 323a +/- 51.t27 276 +/- 44.5.9c +/- 3.Dunnett's Two-Sided Multiple Comparison Test, p < 0.05 tn Vs t1. b Dunnett's Two-Sided Multiple Comparison Test, p < 0.05 tn Vs t6. c Dunnett's Two-Sided Multiple Comparison Test, p <0.05 tn Vs t12.into the rather luteal phase of vascular development (vascular space) with a substantial production of nitric oxide (NO?. Nitric oxide, besides having a radical nature, is an important mediator for vasodilatation, the relaxation of the myometrium, anti-aggregation action and angiogenic stimulation which occurs by means of VEGF (vascular endothelial growth factor); this in turn stimulates NO synthase (NOS) [10], indicating that the NO?is trying to maintain its level with the self-induction Phenyl (4-chloro-3-fluorophenyl)carbamate of NOS. This synthesis, even though it occurs in PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13867361 all menstrual phases as eNOS (endothelial) and iNOS (induced), increases slightly with progestin stimulus [11]. This entire system must be counterbalanced in a very precise manner. Locally, there is also an increase in the SOD that coincides with this increase in the synthesis of NO? SOD, carrying out the dismutation of O?(superoxide), to form 2 H2O2 + O2, inhibits the NO?+ O?reaction that tends to 2 produce the ONOO- ion (peroxynitrite) which, besides having a strong oxidizing strength, removes NO?and limits its availability. Nevertheless, the high level of available NO?can however react with O?, since the reaction 2 between the two is by far the fastest in the body (1 ?10-9 sec) and can generate OS. It is therefore not surprising that the vectorial result of the antioxidant and oxidant production, action of the progestin phase stabilizes on an OS scale. That which occurred in terms of d-ROMs values was seen in all cases analyzed, therefore the data indicating that OS conditions are present for approximately 2/3 of the menstrual cycle phases is considered "solid". The connection between OS and the E2 and P4 levels is 3-(tert-Butyldimethylsilyloxy)propan-1-amine also confirmed by the previous observations, since we know that the levels of hydroperoxide in women taking birth control pills increase significantly [12,13]. This fact must clearly be confirmed through specific studies, but tends to discredit the hypothesis that exogenous estrogens have an antioxidant action [14,15].The opposite instead seems to be true. Hypothetically speaking, the action of the estrogens may be similar to that which occurs during exertion [16]. In this condition, the LDLs are oxidized but are also more easily up-taken by the blood receptors, or kept under control and partially "diminished" by the muscular antioxidant systems. Same has been described by other authors [17] that suggest estradiol promote the oxidation of LDL and promotes their clearance from the liver. If however their quantity increases, even at the rate of an inefficient antioxidant system, they are subject to vascular uptake (sub-endothelial).