Biochemical changes and treatment in glaucoma.

Glaucoma is the second cause of blindness worldwide. This disease is a neurodegenerative disorder characterized by high intraocular pressure, loss of retinal ganglion cells (apoptosis). Even though there is much research done in this field, the results have not yet managed to stop the progression of glaucoma or to heal this pathology. Free oxygen radicals play a major role; they are formed in the aqueous humor and in the vitreous and they produce apoptosis of the neurons in the optic nerve head, degradation of the trabecular meshwork cells. The purpose of the article is to help in trying to understand the physiopathology of glaucoma and the efficacy of its treatments.

Allergic nephritis prevention by prostaglandins E2 and F2 alpha.

The effects of prostaglandins E2 and F2 alpha on renal lesions induced by an anti-rat serum were investigated in rats. It was found that these prostaglandins, administered concomitantly with the antiserum, were able to prevent or remarkably attenuate these lesions. A very interesting finding is that, after prostaglandin administration, no or insignificant morphological alterations of the kidney occurred, in spite of the fact that its mononuclear cell infiltration was somewhat persistent. Hence, in addition to the known effects of these prostaglandins on the immune response components, the blockade of cellular receptors for immunoglobulins is to be considered as a main mechanism in explaining their preventive action in allergic nephritis.

The protective action of prostaglandins E2 and F2 alpha on antibody induced myocardial lesions: morphological studies.

Optic and electron microscopical investigations as well as histochemical investigations were performed in rats which have intraperitoneally received an anti-rat serum together with either PGE2 or PGF2 alpha, in order to study the effect of these prostaglandins on antibody-induced myocardial lesions. PGE2 and, especially, PGF2 alpha were found to considerably prevent the myocardium against these lesions (mononuclear cell infiltration, interstitial and intracellular hyperhydration, disintegration of myofibrils, vacuolization of sarcoplasmic reticulum, mitochondrial swelling and degradation, lysosomal activation and disruption of myocardial sarcolemmas and blood capillary membranes). Their protective actions were revealed in animals killed 24 h and 6 days after the administration of anti-rat immunoglobulins.

Effects of some prostaglandins on the main phosphorylating, electron transporting and peroxidative systems of the erythrocyte membrane.

Investigations regarding the main biochemical systems of the erythrocyte membrane were performed on rat erythrocyte ghosts after treating the animals with PGA1, PGE1 and PGF2alpha. These investigations have shown that the prostaglandins which were found to induce changes in the erythrocyte flexibility (PGE1 and PGF2ALPHA) also induce significant changes in the concentrations of lipid peroxides, SH groups, proteins and nicotinamide adenine nucleotides, as well as in the activity of some electron transportors belonging to the nicotinamide proteins, in the erythrocyte membrane.

Effects of cobalt-60 gamma-irradiation in association with prostaglandin E1 treatment on the cyclic AMP levels of some radiosensitive tissues.

The amounts of cyclic AMP in brain, liver and intestinal mucosa have been measured in rats, at constant intervals, up to 18 days after whole-body exposure to either a unique moderate dose (500 rd) or a unique lethal dose (750 rd) of cobalt-60 gamma-radiation in association with a preliminary intraperitoneally treatment with prostaglandin E1 (5 microgram/100 g body weight/day) during five days. The amounts of tissular cyclic AMP in these two experimental groups were compared with those obtained from control groups identically irradiated or treated with prostaglandin E1. The effects of gamma-irradiation and prostaglandin E1 treatment on the cyclic AMP levels were found to be quite specific in these organs, suggesting that they contain different adenyl cyclase-cyclic AMP-phosphodiesterase systems: a cerebral system which is influenced by both gamma-radiation and prostaglandin E1, a hepatic system which is "radioresistant" and an intestinal system which is not influenced by prostaglandin E1. When associated with gamma-radiation, this prostaglandin is capable, on the one hand, to annul the "radioresistance" of the hepatic cyclic AMP system and, on the other hand, to annul the "radiosensitivity" of the intestinal cyclic AMP system.

Dynamics of the changes in the cerebral amounts of cyclic AMP and some prostaglandins during cobalt-60 gamma-radiation-induced brain edema.

The total amounts of cyclic AMP (cAMP), prostaglandin E1 (PGE1) and prostaglandin F2alpha (PGF2alpha) in cerebra have been measured in rats, at constant intervals, up to 18 days after whole body exposure to either a unique moderate dose (500 rads) or a unique lethal dose (750 rads) of cobalt-60 gamma-radiation. The experimental findings indicate that this radiation (i) results in an abrupt short-lasting increase in the amount of cerebral cAMP after a 500 rad-irradiation and a progressive long-lasting increase in its amount after a 750 rad-irradiation, and (ii) induces no change in the normally, existing correlation between cerebral PGE1 and cAMP, but affects deeply the normally existing correlation between cerebral PGF2alpha and cAMP. These biochemical alterations generally parallel the evolution of the radiation-induced brain edema.

Tissular cycli AMP levels after treatments with prostaglandins.

In this study both prostaglandin A1 (PGA1) and prostaglandin F2alpha (PGF2alpha) have been shown to be effective long-lasting stimulators of the cyclic AMP (cAMP) synthesis in the liver, intestinal mucosa and brain, whereas prostaglandin E1 (PGE1) was found to have a similar effect on the cerebral cAMP synthesis and a dissimilar effect (decrease) on the hepatic one. A lack of sensitivity of the intestinal mucosa cAMP to PGE1 was also observed.