Structural features of PGBX (a prostaglandin polymer) deduced by analogies with dimers derived from 15-keto-prostaglandin B.

The polymeric prostaglandin, PGBX, has a beneficial effect on oxidative phosphorylation of damaged mitochondria in vitro and has manifested interesting effects in vivo. Its chemical structure has been partially elucidated by comparison of its 13C-NMR (nuclear magnetic resonance) spectrum with the spectra of prostaglandin monomers. Reported here is subsequent comparison of PGBX with two prostaglandin dimers derived from 15-keto-PGB1, which provide more complete structural information. The two prostaglandin dimers were synthesized and analyzed by 13C-MNR and by other techniques, with particular attention to positions of linkages between the two monomeric prostaglandin subunits of the dimers. Based on these data, some proposals are presented regarding probable locations of linkages between prostaglandin monomeric subunits in the polymeric PGBX.

Mechanism of polymeric prostaglandin PGBx for in vitro stabilization of rat liver mitochondrial oxidative phosphorylation.

The mechanism of the in vitro PGBx effect on mitochondria was studied by determining the specific requirements of the assay system composition. These studies showed that (a) rat liver mitochondria must first be exposed to hypotonic media containing PGBx under aerobic conditions, (b) oxygen, Pi, Mg++, phosphate acceptor (nucleotides), and some oxidizable substrates are essential components to yield optimal phosphorylation values. KCl and bovine serum albumin are non-essential components. With regard to nucleotide acceptor specificity, the AMP, ADP, and glucose-ADP-hexokinase systems were satisfactory. With regard to substrate specificity, only beta-hydroxybutyrate and externally reduced NAD+ were unsatisfactory. The requirement for oxygen was twofold: (a) as an absolute requirement for oxidative phosphorylation, and (b) as a requirement for the hypotonic degradation of mitochondria. These results suggest that PGBx reacts with mitochondria to "protect" against degradation during aerobic hypotonic exposure.