dinoprost and Cataract

Oxidative stress and inflammation may be involved in the etiology of age-related cataract. This study is the first to investigate the association between urinary levels of 8-iso-prostaglandin F₂α (PGF₂α; as a biomarker for systemic oxidative stress in vivo) and 15-keto-dihydro-PGF₂α (as a biomarker for systemic inflammation in vivo) and risk of age-related cataract. We observed in a nested case-control study, including 258 women with incident cataract diagnosis and/or cataract extraction and 258 women without cataract, matched on age and date of urine sample collection that, women with higher levels of urinary 8-iso-PGF₂α as compared with lower levels had an increased risk of age-related cataract. There was no difference in 15-keto-dihydro-PGF₂α levels between cases and controls. Our observations lead to the hypothesis that higher systemic oxidative stress increases the risk of developing age-related cataract.

Topics: Aged; Aging; Case-Control Studies; Cataract; Dinoprost; Female; Humans; Inflammation; Oxidative Stress

Topics: Aged; Case-Control Studies; Cataract; Dinoprost; Exfoliation Syndrome; Female; Humans; Immunoenzyme Techniques; Male

To understand the role of prostaglandins F(2alpha) and E(2) in aqueous humor under the normal condition, their concentrations were measured by enzyme immunoassay in aqueous fluid obtained from either eye of 60 patients during cataract surgery and correlated with clinical factors as the age and intraocular pressure. The concentrations of prostaglandin F(2alpha) in the aqueous of all patients were below the level of detection. The concentrations of prostaglandin E(2) in the aqueous were below the level of detection in 37 patients while ranged from 9 to 48 pg/mL (median, 31) in 23 patients. The levels of prostaglandin E(2) did not have correlation with the age of the patients or the intraocular pressure of the eyes. In conclusions, the concentrations of prostaglandin E(2) were apparently higher than the concentrations of prostaglandin F(2alpha) in the aqueous. This study could not prove the relationship between prostaglandin levels and the intraocular pressure or the age.

Topics: Adult; Aged; Aged, 80 and over; Aging; Aqueous Humor; Cataract; Cataract Extraction; Dinoprost; Dinoprostone; Female; Humans; Intraocular Pressure; Male; Middle Aged

The authors investigated the concentrations of 8-isoprostaglandin F(2a), a marker of oxidative stress in vivo, and ascorbic acid, a protectant against oxidative damage, in the aqueous humour of patients with exfoliation syndrome (XFS) and cataract and compared the results with those in age matched patients with cataract, but without XFS, to determine whether XFS is associated with increased oxidative stress.. Aqueous humour was aspirated at the beginning of phacoemulsification cataract surgery from 27 eyes of 27 cataract patients with XFS and 27 eyes of 27 age matched cataract patients without XFS. 8-Isoprostaglandin F(2a)concentration in the aqueous was determined with a commercial immunoassay; ascorbic acid concentration was measured with a microplate assay method.. The mean concentration of 8-isoprostaglandin F(2a)in the aqueous from patients with XFS (2429 (SD 2940) pg/ml; range 400-10500 pg/ml) was significantly higher than that measured in the aqueous of age matched control patients (529.1 (226.8) pg/ml; range 325-1000 pg/ml); (p = 0.0028). Furthermore, mean ascorbic acid concentration in XFS patients (0.75 (0.39) mM; range 0.28-1.70 mM) was significantly lower than that found in control patients (1.19 (0.47) mM; range 0.53-2.4 mM); (p = 0.0005). There was a reverse correlation between 8-isoprostaglandin F(2a)and ascorbic acid concentration.. 8-Isoprostaglandin F(2a)was significantly increased in the aqueous of patients with XFS, and ascorbic acid was decreased, providing evidence of a role for free radical induced oxidative damage in the pathobiology of XFS.

Topics: Antioxidants; Aqueous Humor; Ascorbic Acid; Cataract; Dinoprost; Exfoliation Syndrome; F2-Isoprostanes; Free Radical Scavengers; Humans; Immunoassay; Oxidative Stress; Prospective Studies

Previous work has shown that exposure of lens epithelial cells or rabbit eyes in vivo to ultraviolet B (UVB) radiation enhanced prostaglandin (PG)E2 synthesis. Such enhanced PGE2 synthesis was related to the increased DNA synthesis that followed UVB exposure. The current study examined the relationship between enhanced prostaglandin synthesis and UVB-induced cataract formation.. Seventy albino (New Zealand white) rabbit eyes were exposed to UVB radiation in vivo. Fluence of radiation at the cornea was 2.8 J/cm2, 5.6 J/cm2, or 11.2 J/cm2. Eyes were examined 24 hours after UVB exposure and for as long as 10 days by slit lamp biomicroscopy. Mass spectrometry was used to measure PGE2, PGF2 alpha, and 6-keto-PGF1 alpha content of the lens and iris-ciliary body using authentic standards. To determine the effect of inhibition of prostaglandin synthesis on UVB-induced cataract formation, animals were given indomethacin intraperitoneally. Other pharmacologic agents, such as PGE2, PGF2 alpha, and misoprostol, were applied topically to the eye. The effect of UVB on K+ pump was determined by incubating isolated lenses with [86Rb+].. Twenty-four hours after UVB exposure, PGE2 and PGF2 alpha concentrations in aqueous humor were increased by 100- and 30-fold, respectively. Lens PGE2 and PGF2 alpha increased by 6- and 4-fold, respectively, after UVB radiation exposure. Pretreatment of animals with indomethacin prevented the rise in lens and aqueous humor PGE2 and PGF2 alpha levels. Furthermore, indomethacin was partially protective against UVB cataract formation and lowered cataract severity from stage 3 to stage 1, but it did not prevent UVB-induced lens changes completely. Topical application of PGE2 before UVB exposure completely prevented cataract formation in the UVB-exposed eye. In contrast, topical administration of PGF2 alpha increased cataract severity. UVB-induced cataract formation preceded changes in [86Rb]+ uptake in lenses subsequently incubated in K(+)-free Tyrode's.. Enhanced synthesis of cyclooxygenase products of arachidonic acid metabolism in the lens is associated with UVB-induced cataract formation in albino rabbit eyes, and inhibition of cyclooxygenase by indomethacin decreased the severity of cataracts. PGE2, the principal arachidonic acid metabolite, appears to have a protective role because pretreatment of the eye with topical PGE2 completely prevented UVB-induced cataract formation, whereas PGF2 alpha increased the severity of the cataract. The evidence presented for a role of PGF2 alpha in the development of cataract suggests that caution be exercised in the use of PGF2 alpha derivatives in the therapy of glaucoma.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Cataract; Ciliary Body; Conjunctiva; Cornea; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Indomethacin; Iris; Lens Cortex, Crystalline; Misoprostol; Ophthalmic Solutions; Oxytocics; Potassium; Rabbits; Radiation Injuries, Experimental; Rubidium Radioisotopes; Sodium-Potassium-Exchanging ATPase; Ultraviolet Rays

The relationship between the development of galactose-induced cataractogenesis and rat lens microsomal prostaglandin (PG) biosynthesis was studied. Within 24 hr of the introduction of 50% galactose to the rat's diet, lens PGF2 alpha production fell dramatically to 31% of control. Following the initial depression of PGF2 alpha biosynthesis, the ability to generate PGF2 alpha in lens microsomes slightly recovered reaching 58- and 53% of controls at day 2 and day 5 on the sugar diet, respectively. Determination of microsomal PGF2 alpha biosynthesis at 9- and 21 days revealed a continued decline in PG synthesis with complete cessation of PGF2 alpha synthesis by day 36 (hypermature cataracts, +5). The decreased PGF2 alpha biosynthetic capacity was a result of decreased cyclo-oxygenase activity since: PGE2 production demonstrated a similar time course for inhibition; and lens microsomes from control and galactose fed rats revealed no difference in the PGs produced from PGH2 endoperoxide. Neither galactose (1 mM) nor galactitol (1 mM), when added to control microsomal preparations inhibited PG biosynthesis, eliminating the possibility of a direct effect of the sugar, or its metabolite, on cyclo-oxygenase activity. While PG biosynthesis was rapidly inhibited by the galactose feeding no changes were observed in basal lens cyclic AMP levels measured during the first 5 days of the feedings. These results demonstrate that depressed PG biosynthesis is an early consequence of galactose feeding.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Cataract; Cyclic AMP; Dinoprost; Dinoprostone; Galactose; Lens, Crystalline; Male; Microsomes; Prostaglandin D2; Prostaglandin Endoperoxides, Synthetic; Prostaglandin H2; Prostaglandins; Prostaglandins D; Prostaglandins E; Prostaglandins F; Prostaglandins H; Rats; Rats, Inbred Strains

Vitreous samples were obtained from 41 eyes undergoing vitrectomy, and radioimmunoassays were performed to measure concentrations of the prostaglandins PGE2, PGF2 alpha, prostacyclin, and thromboxane. Presumably physiological levels (approximately 100 picograms/ml) were found in vitreous from eyes undergoing cataract extraction. Eyes with vitreous haemorrhage, retinal detachment, or cystoid macular oedema had similarly low levels. Vitreous prostaglandins were mildly elevated in trauma and endophthalmitis and markedly elevated in aphakic bullous keratopathy. The role prostaglandins may play in cystoid macular oedema is reviewed.

Topics: Adult; Aged; Cataract; Dinoprost; Dinoprostone; Female; Humans; Macular Edema; Male; Middle Aged; Prostaglandins; Prostaglandins E; Prostaglandins F; Retinal Detachment; Thromboxanes; Vitreous Body