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Biomedical subjects

F Simonelli

Publications and source records attributed to F Simonelli.

17 recordsLinked to original sources
PubMed1992

Galactokinase activity in patients with idiopathic presenile and senile cataract.

The activity of galactokinase in red blood cells of 30 patients affected by idiophatic presenile and senile cataract, and of 20 age-matched controls with perfectly transparent lenses, was investigated. The results obtained show a partial deficiency of the galactokinase activity in the patients affected by presenile idiopathic cataract. There is, moreover, a significant relationship between the cortical form of cataract and enzymatic reduction.

Adult↗
PubMed1991

Cataract risk factors: blood level of antioxidative vitamins, reduced glutathione and malondialdehyde in cataractous patients.

Since many years experimental evidences have suggested an association between nutrition and lens opacities. A dietary deficiency of antioxidants and reactive oxygen scavengers may be involved in the pathogenesis of the "idiopathic" human senile cataract, as it has been demonstrated in some experimental cataracts. We tested the levels of ascorbic acid (vit. C), alpha-tocopherol (vit. E), reduced glutathione (GSH) and malondialdehyde (MDA) in the plasma or in the red blood cells (RBC) of 42 patients who were affected by surgically significant cataract and of 40 age-matched controls. Plasma vit. C mean level was 4.46 gamma/ml in cataracts and 4.62 gamma/ml in controls, while vit. E level was 7.70 and 7.09 gamma/ml respectively. RBC GSH was found to be 342 gamma/ml in cataracts and 346 in controls, while the MDA content was 4.06 picoMol/ml and 4.08 picoMol/ml respectively. The level of each tested nutrient or metabolite was not found to be statistically different between cataractous patients and controls, nor any significant trend was found to be present when the nutrients and metabolites were correlated to each other. Our results do not support the hypothesis of a nutritional deficiency in human senile cataracts. However, a defect in the antioxidative metabolism pathways could be present either systemically or at lens level.

Age Distribution↗
PubMed1990

Systemic human diseases as oxidative risk factors in cataractogenesis. II. Chronic renal failure.

In this study we have investigated the oxidative metabolism of red cells (RBC), plasma, serum and aqueous humour of healthy subjects and of age-matched cataractous patients with and without chronic renal failure (CRF). Reduced glutathione (GSH) levels in RBC were lower in CRF patients than in the other groups. Oxidized glutathione (GSSG) plasma levels in CRF patients were higher than those of controls and cataractous subjects. The activity of the enzyme glucose-6-phosphate dehydrogenase in RBC was significantly reduced in CRF patients with respect to the other two groups. The levels of malondialdehyde (MDA) in RBC and in lens were about twice in CRF patients compared with the other two groups. The plasma levels of vitamin E were diminished in CRF patients; on the contrary, the biological liquid oxidant activity (BLOA) of serum in CRF patients was significantly higher than in controls and in cataractous patients without CRF. Cataractous patients with and without CRF showed similar levels of GSH in aqueous humour; on the contrary, the content of GSSG was significantly higher in CRF patients. Our findings seem to demonstrate that CRF patients are exposed to oxidative stresses that could probably act synergistically with uraemia and carbamylation of lens proteins. This synergism could explain why CRF represents a relatively high risk factor for cataract.

Aged↗
PubMed1990

The decrease of free epsilon-amino groups in senile and diabetic cataracts.

Free epsilon-amino groups in soluble and insoluble proteins were measured in clear human lenses and in diabetic and nondiabetic senile cataractous lenses. The free epsilon-amino group content of soluble and insoluble proteins was significantly lower in diabetic cataracts than in clear lenses and nondiabetic senile cataracts. Our results seem to demonstrate that nonenzymatic glycosylation of lens proteins could play a role in the pathogenesis of diabetic cataract.

Adult↗
PubMed1990

[Hydrogen peroxide in the aqueous humor and cataract formation in human diabetes].

Hydrogen peroxide in the aqueous humor was measured in cataractous eyes from normal subjects and in cataractous eyes from diabetic subjects. The level of H2O2 in the aqueous humor was significantly higher in diabetes than in the idiopathic forms. It is likely that in the eye, impaired enzymic defenses lead to the accumulation of reactive species of O2, such as H2O2, which induces lipid peroxidation. This mechanism may be involved, as a direct consequence of retinal damage, in the pathogenesis of cataract in diabetes.

Aqueous Humor↗
PubMed1990

[Measurement of the erythrocyte galactokinase activity in patients with presenile and senile idiopathic cataract. Preliminary study].

The activity of galactokinase in red blood cells, has been assayed in 17 patients with idiopathic senile and presenile cataract and in 12 age-matched subjects with perfectly transparent lenses. 3 of the idiopathic cataract patients (17.6%) showed low erythrocytes GK activity, while nobody in the control group showed reduced GK activity. Although preliminary, our results seem to support the possibility that a chronic disorder of galactose metabolism may be involved in the pathogenesis of the idiopathic senile and presenile cataract.

Adult↗
PubMed1990

[Possible role of altered levels of plasma docosahexaenoic acid in the pathogenesis of retinitis pigmentosa. Preliminary results].

Plasma samples obtained from Retinitis Pigmentosa (R.P.) patients and controls were assayed for docosahexaenoic acid (DXA), the major fatty acid in photoreceptor cells, in order to evaluate the possibility that abnormalities in PUFA metabolism could be involved in R.P. pathogenesis. Our preliminary results show levels of plasma DXA in dominantly inherited R.P. lower than in the recessive forms and controls.

Docosahexaenoic Acids↗
PubMed1989

Lipid peroxidation and human cataractogenesis in diabetes and severe myopia.

To investigate the role of lipid peroxidation in human cataract, malondialdehyde, a breakdown product of lipid peroxidation, was measured in clear and cataractous lenses from normal subjects, and in cataractous lenses from diabetics and from subjects with severe myopia. The cataractous lenses contained more malondialdehyde than did clear lenses and the level was higher in diabetes and severe myopia than in the idiopathic forms. This indicates that lipid peroxidation may be involved in the development of senile cataract and, as a direct consequence of retinal damage, also in the pathogenesis of cataract in diabetes and in severe myopia.

Adult↗
PubMed1989

[Role of the non-enzymatic glycosylation of protein in the formation of human cataracts].

We have measured the free epsilon amino groups in soluble and insoluble proteins of clear human lenses and diabetic and non-diabetic senile cataractous lenses. The free epsilon amino groups content of soluble and insoluble proteins was significantly lower in diabetic cataracts than in clear lenses and non diabetic senile cataracts. Our results seem to demonstrate that non-enzymatic glycosylation of lens protein could play a role in the pathogenesis of cataract in diabetes.

Adult↗
PubMed1989

[Lipid peroxidation and cataract formation in experimental diabetes].

To investigate the role of lipid peroxidation in diabetic cataractogenesis, malondialdehyde, a breakdown product of lipid peroxidation, was measured in lenses with incipient opacities and in retinas from diabetic rats and in clear lenses and in retinas from normal rats. The malondialdehyde mean values obtained in the transparent and cataractous lenses showed non-significant differences, while non-diabetic rat retinas had a significantly lower mean level of malondialdehyde compared with diabetic rat retinas (p less than 0.01). This indicates that, in streptozotocin-induced diabetic rats, lipid peroxidation is apparently not involved in the development of cataract, but it is quite probably involved in retinal damage. The retina, richer in polyunsaturated fatty acids than other ocular structures, is the elective site of lipid peroxidation and from this membrane peroxidation products might probably diffuse and damage other ocular tissues.

Animals↗
PubMed1988

Systemic human diseases as oxidative risk factors in cataractogenesis. I. Diabetes.

In this study we have investigated the oxidative metabolism of red blood cells (RBC), plasma, serum, aqueous humor, and lens of healthy subjects and of age-matched cataractous patients with and without diabetes. Reduced and oxidized glutathione (GSH GSSG) levels in RBC were similar among the three groups. Plasma levels of GSSG were higher in diabetics than in cataractous and control subjects. No differences in plasma content of GSH were noted among the three groups. The activity of the enzyme glucose-6-phosphate dehydrogenase was significantly diminished in diabetic patients. Controls and cataractous patients showed similar levels of malondialdehyde (MDA). Although not significant the MDA content in RBC from diabetics was elevated. No differences in plasma levels of vitamin E were noted among the three groups. The biological liquid oxidant activity of serum in diabetic patients was significantly higher than in controls and cataractous patients. GSH levels in aqueous humor were similar in diabetic and nondiabetic cataractous patients. The content of GSSG in aqueous humor was highest in diabetic patients. Control clear lenses showed low levels of MDA. The MDA levels in cataractous lenses from nondiabetic patients were significantly higher than those of controls. In diabetic patients the content of MDA in the lens was approximately twice as high as the cataractous values. Our results seem to demonstrate that oxidative damage could play a role in the pathogenesis of cataract in diabetes.

Adult↗
PubMed1987

Cataract formation in diabetic patients and galactose-1-phosphate uridyltransferase deficiency.

We have evaluated the levels of red blood cell galactose-1-phosphate uridyltransferase in 20 patients with cataract and in 15 subjects without cataract, suffering from compensated, noninsulin-dependent, type II diabetes. The diabetic patients were compared with a previously examined group of 65 age-matched nondiabetic subjects (25 of whom suffered from bilateral idiopathic cataract). In diabetic patients, the average galactose-1-phosphate uridyltransferase levels tended to be lower and the percentage of cases of reduced enzymatic activity tended to be higher than in the corresponding nondiabetic subjects.

Adult↗
PubMed1987

Galactose-1-P-uridyl transferase activity in patients with congenital and infantile cataract.

The activity of red blood cell galactose-1-P-uridyl transferase in 22 patients with congenital and infantile cataract and in 18 age-matched controls was investigated. All control subjects examined showed normal enzymatic levels, while 31.8% of patients with congenital and infantile cataract presented a statistically significant reduced enzymatic activity (mean--2 SD in controls). Twenty-four parents of children with congenital and infantile cataract were also examined. Four parents were affected by congenital cataract and the other 20 showed transparent lenses. The parents were compared with a group of 20 age-matched control subjects examined previously. There was no difference in the average enzymatic activities between the groups. The results suggest that a chronic disorder of galactose metabolism may be involved in the development of congenital and infantile cataract.

Cataract↗
PubMed1986

Possible role of galactose-1-P-uridyl transferase activity deficiency in red blood cells in the development of the presenile and senile cataract.

The activity of red blood cells galactose-1-P-uridyl transferase in 64 patients with presenile and senile cataracts (nondiabetics) and in 41 age-matched controls was investigated. All control subjects examined have shown normal enzymatic levels, while 21.9% of patients with presenile cataracts and 21.7% of patients with senile cataracts presented a statistically significant reduced enzymatic activity (mean +/- 2 SD in controls).

Adult↗
PubMed1985

Red blood cells galactose-1-P-urydil transferase in senile and presenile cataracts.

There are conflicting reports in the literature regarding the role of partial deficiency of "galactosemic" enzymes (galactose-1-P-urydil transferase and galactokinase) in the development of infantile and presenile cataract. The AA. have investigated the levels of Red Blood Cell Galactose-1-P-urydil transferase in 39 cataractous patients and in 22 age matched controls. A weak correlation between the enzymatic activity deficiency and the presenile cataract has been identified. The results suggest that a chronic impairment of galactose metabolism may be a contributory risk factor in the pathogenesis of presenile cataracts; however, further investigations are required to assess the actual significance of the findings of the present paper.

Adult↗