[tanysquirrel]

could this be the reason WHY bovine ovary works ?

https://en.wikipedia.org/wiki/Adrenodoxin_reductase

NADPH:adrenodoxin oxidoreductase, mitochondrial also known as adrenodoxin reductase is an enzyme that in humans is encoded by the FDXR gene, also known as ADXR. It catalyzes the following reaction:

NADPH + 2 oxidized adrenodoxin —→ 2 reduced adrenodoxin + NADP+ + H+

In both bovine and human genomes there is only a single copy of this gene.[1]

ADXR gene is expressed in all tissues that have mitochondrial P450s. The highest levels of the enzyme is found in the adrenal cortex, granulosa cells of the ovary and leydig cells of the testis that specialize in steroid hormone synthesis.[2] In addition the enzyme is also expressed in the liver, the kidney and the placenta.

Function[edit]

Adrenodoxin reductase is a mitochondrial flavoprotein as it carries a FAD type coenzyme. The enzyme functions as the first electron transfer protein of mitochondrial P450 systems such as P450scc. The FAD coenzyme receives two electrons from NADPH and transfers them one at a time to the electron transfer protein adrenodoxin.[3] Adrenodoxin functions as a mobile shuttle that transfers electrons between ADXR and mitochondrial P450s.[4]

Adrenodoxin reductase has been also called a ferredoxin-NADP+ reductase. But, determination of the sequence and structure of the enzyme revealed that it is completely different from ferredoxin reductase

Ferredoxin—NADP(+) reductase:
'Ferredoxin: NADP+ reductase is the last enzyme in the transfer of electrons during photosynthesis from photosystem I to NADPH.[1] The NADPH is then used as a reducing equivalent in the reactions of the Calvin cycle.[1] Electron cycling from ferredoxin to NADPH only occurs in the light in part because FNR activity is inhibited in the dark.[10] In nonphotosynthetic organisms, the FNR primarily works in reverse to provide reduced ferredoxin for various metabolic pathways. These pathways include nitrogen fixation, terpenoid biosynthesis, steroid metabolism, oxidative stress response, and iron–sulfur protein biogenesis.[6]'

P450scc:
Cholesterol side-chain cleavage enzyme is commonly referred to as P450scc, where "scc" is an acronym for side-chain cleavage. P450scc is a mitochondrial enzyme that catalyzes conversion of cholesterol to pregnenolone. This is the first reaction in the process of steroidogenesis in all mammalian tissues that specialize in the production of various steroid hormones
The highest level of the cholesterol side-chain cleavage system is found in the adrenal cortex and the corpus luteum.[2] The system is also expressed at high levels in steroidogenic theca cells in the ovary, and Leydig cells in the testis.[2] During pregnancy, the placenta also expresses significant levels of this enzyme system.[4] P450scc is also present at much lower levels in several other tissue types, including the brain.[5] In the adrenal cortex, the concentration of adrenodoxin is similar to that of P450scc, but adrenodoxin reductase is expressed at lower levels

In each steroidogenic cell, the expression of the P450scc system proteins is regulated by the trophic hormonal system specific for the cell type.[2] In adrenal cortex cells from zona fasciculata, the expression of the mRNAs encoding all three P450scc proteins is induced by corticotropin (ACTH).[8][17] The trophic hormones increase CYP11A1 gene expression through transcription factors such as steroidogenic factor 1 (SF-1), by the α isoform of activating protein 2 (AP-2) in the human, and many others.[17][18] The production of this enzyme is inhibited notably by the nuclear receptor DAX-1

DAX1 (dosage-sensitive sex reversal, adrenal hypoplasia critical region, on chromosome X, gene 1) is a nuclear receptor protein that in humans is encoded by the NR0B1 gene (nuclear receptor subfamily 0, group B, member 1).[2][3][4] The NR0B1 gene is located on the short (p) arm of the X chromosome between positions 21.3 and 21.2, from base pair 30,082,120 to base pair 30,087,1DAX1 plays an important role in the normal development of several hormone-producing tissues. These tissues include the adrenal glands above each kidney, the pituitary gland and hypothalamus, which are located in the brain, and the male and female reproductive structures (the testes and ovaries). DAX1 controls the activity of certain genes in the cells that form these tissues during embryonic development. Proteins that control the activity of other genes are known as transcription factors. DAX1 also plays a role in regulating hormone production in these tissues after they have been formed.


so , in theory, this may explain the "b.o. point of no return" as it is expressed in the brain as well, the "rewiring" we all talk about? interesting, more research needed, I think..