Steroidogenic tissue can respond almost immediately to a stimulatory hormonal stimuli.
Recent findings are shedding light on the molecular and cellular mechanisms that are
used to synthesize and export steroid hormones in the acute phase of stimulation.
In addition to utilising the cAMP intracellular messenger system to convey a stimulatory
message, steroidogenic cells may employ the protein kinase C, arachidonic acid, tyrosine
phosphate and nitrous oxide systems. It has been proposed that cholesterol laden vesicles
travel along a network of intermediate filaments to reach the mitochondria. Cholesterol
may then translocate from the outer mitochondrial membrane to the inner via sites
of contact between the two membranes. These contact sites may be composed of protein
bridges which include the constituents, porin, the benzodiazepine receptor and GTP
binding proteins. Cholesterol is transported through the contact sites to the inner
membrane and on reaching cytochrome P450 side chain cleavage (P450scc), cholesterol
is converted to pregnenolone. Pregnenolone is in turn converted to a range of steroid
hormones via enzyme casades. GTP binding proteins may regulate the contact site between
the inner and outer membranes and thereby modulate cholesterol flux to P450 scc. In
the adrenal and gonads the rate that cholesterol traverses the contact point to reach
the inner membrane is accelerated by the Steroidogenic acute regulatory protein. Newly
synthesized steroid hormones are transported to the cell periphery for export via
a mechanism that may utilise an ion exchange protein.
Key words
Steroidogenesis - Steroidogenic Acute Regulatory Protein - Sterol Carrier Protein
- Endozepine - Steroidogenic Factor 1 - Porin
