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Biomedical subjects

G Auricchio

Publications and source records attributed to G Auricchio.

At least 19 recordsLinked to original sources
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

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↗
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↗
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

Effect of topical glucocorticoid administration on the protein and nonprotein sulfhydryl groups of the rabbit lens.

The effects of topical administration of glucocorticoids on rabbit lenses are described. Animals were divided into three groups. The first group (A) served as control, the second (B) and the third (C) group were treated with betamethasone and fluorometholone, respectively. After 40 days of treatment there was a significant fall in the levels of nonprotein sulfhydryl (-SH) groups (group A: 3.82 +/- 0.21; group B: 2.61 +/- 0.11; group C: 1.93 +/- 0.13 mumol/lens) and of protein -SH groups (group A: 8.215 +/- 1.023; group B: 4.120 +/- 0.631; group C: 4.068 +/- 0.538 mumol/lens). Also ascorbic acid levels showed a significant decrease both in lens and in aqueous humor. No differences were noted in the reduced glutathione content in aqueous humor. The fall in nonprotein and protein -SH could be the first event in the well-known biochemical changes that occur in steroid-induced cataract. The mechanism underlying steroid-induced damage could be due to a conformational change of lens crystallins which results in an unmasking of -SH groups with a consequent increased susceptibility to oxidation. The decrease of ascorbic acid should represent an effect of the fall in the glutathione system. Lastly, it is hypothesized that the protective effect exerted by some substances, such as vitamin E and ascorbic acid, occurs by counteracting this oxidation.

Administration, Topical↗
PubMed1986

Effect of vitamin E on glutathione content in red blood cells, aqueous humor and lens of humans and other species.

High doses of orally administered vitamin E have been given to humans, rabbits and rats. Placebo has been given to control groups. At the end of the treatment period, enhanced levels of reduced glutathione (GSH) were found in the red blood cells (humans and rabbits), aqueous humor (humans and rabbits) and lens (rabbits and rats) of treated subjects and animals. The percentage of GSH converted to oxidized glutathione (GSSG) was the same in both vitamin E-supplied and control groups. The GSSG--GSH ratio remained unchanged. The plasma levels of vitamin E were significantly higher in treated than in control subjects and animals. At the end of the study, the levels of vitamin E in aqueous humor and lens of rabbit were the same in animals which received vitamin E and in animals which received placebo. Lastly, vitamin E administration did not influence ascorbic-acid levels in plasma (humans and rabbits), aqueous humor, lens and vitreous body (rabbits).

Animals↗
PubMed1985

In vitro effect of alpha-tocopherol on lysophosphatidylcholine-induced lens damage.

Lysophosphatidylcholine (LPC) has been shown to be toxic to the lens in organ culture. An investigation into whether vitamin E counteracts the in vitro damaging effect of LPC on rat lenses was undertaken. A concentration higher than 10 micrograms ml-1 LPC in the culture medium is necessary to damage rat lenses, as assessed by protein content of the medium and Na+ and K+ content of the lens. Vitamin E affords its protection when present at a concentration of 10(-3) M: both the protein efflux from the lens and the lenticular cation imbalance are prevented, also if LPC concentration is 100 micrograms ml-1. This effect may be due more to the physicochemical properties of vitamin E in the stabilization of biological membranes, than to its chemical behaviour as an antioxidant.

Animals↗
PubMed1985

Vitamin E and red blood cell glutathione.

High doses of orally administered vitamin E (1000 IU/day) have been given to ten normal volunteers. Ten control subjects received placebo. Red blood cell glutathione was significantly higher in treated subjects than in the controls (controls: 267.5 +/- 15.7 micrograms/mL; treated: 374.8 +/- 17.3 micrograms/mL). These findings could be explained by an increase of glutathione synthesis brought about by the stimulation of glutathione synthetase activity. An alternative possibility is a reduced utilization of glutathione for the detoxification of free radicals. These two mechanisms could be effective in counteracting the glutathione content feedback of the synthetizing enzymes.

Adult↗
PubMed1985

Changes of some biochemical parameters of the lens in galactose-treated weaned rats with and without vitamin E therapy.

We tried to counteract the appearance of galactosemic cataracts in weaned rats by high doses of vitamin E. Rats were fed a diet containing 33% galactose. Cataract development was monitored by biomicroscopy and by several biochemical parameters: K+/Na+ ratio, aldose reductase activity, level of protein and non-protein sulfhydryl (SH) groups. Vitamin E was given parenterally at a dose of 100 mg/kg/day. The K+/Na+ ratio drops after 15 days of galactosemia, while the level of the aldose reductase rises after only 5 days of treatment. The non-protein SH groups lens contents fall from the 5th day of treatment onwards, while protein SH groups are not affected. In short-term experiments vitamin E does not prevent biochemical changes caused by galactosemia. The oxidative insult does not seem to be primarily involved in galactose cataract.

Aldehyde Reductase↗
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↗