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J P Freitas

Publications and source records attributed to J P Freitas.

At least 19 recordsLinked to original sources
PubMed1998

Oxidative stress in Adamantiades-Behçet's disease.

BACKGROUND: Adamantiades-Behçet's disease is a chronic systemic disorder associating oral and genital ulcerative lesions with ocular and cutaneous manifestations. Previous publications report increased superoxide production by neutrophils and macrophages, increases in cytokines and malondialdehyde (MDA), as well as low levels of enzymatic antioxidant defenses. AIM: We looked for another marker of oxidative stress in Adamantiades-Behçet's disease: the presence of clastogenic factors (CF) in patients' plasma. In addition, we determined plasma endproducts of lipid peroxidation (MDA). PATIENTS AND METHODS: We studied 20 patients and 20 controls. The clastogenic activity was evaluated by means of cytogenetic methods. This test (CF test) detects circulating prooxidants, due to their clastogenic effects after exposure of lymphocyte cultures of healthy persons to plasma ultrafiltrates from patients. The clastogenic prooxidants are lipid peroxidation products and cytokines, in particular TNF-alpha. Lipid peroxidation was evaluated by the Yagi method. RESULTS: The CF test was positive in 18 out of 20 patients, while it was negative in all 20 control persons. The mean increase in chromosomal breaks was 10.6 +/- 3.8 in cultures exposed to patients' plasma and 1.3 +/- 2.4 for cultures receiving control plasma (p <0.001). The clastogenic effect of patients' plasma ultrafiltrates was significantly inhibited by superoxide dismutase (EC 1.15.1.1), suggesting an important role of the superoxide radical in the clastogenic pathway. Thiobarbituric-acid-reactive substances (expressed as nanomoles MDA per milliliter) were also significantly increased in these patients: 10.6 +/- 3.2 for patients and 6.6 +/- 1.4 for controls (p <0.001). CONCLUSION: The presence of CF in the plasma of patients, indicating the presence of circulating prooxidants with chromosome-damaging effects, confirms an oxidative stress in Adamantiades-Behçet's disease. The anticlastogenic effect of superoxide dismutase in vitro suggests the implication of the superoxide radical. MDA levels were also significantly increased in patients.

Adolescent↗
PubMed1997

Lipid peroxidation in type 2 normolipidemic diabetic patients.

Vascular complications, as a consequence of atherosclerosis, are the main causes of morbidity and mortality in diabetes. Low density lipoprotein (LDL) oxidation is accepted as a relevant pathogenic mechanism in atherogenesis. The aim of this work was to study the relationship between lipid peroxidation (LPO) and metabolic control. LPO was evaluated in 40 type 2 normolipidemic diabetic patients by measuring thiobarbituric acid reactive substances (TBARS), in the plasma, using malondialdehyde (MDA), end product of the oxidation of polyunsaturated fatty acids, as a standard. Fast blood glucose (FBG), serum total cholesterol (TC) and serum triglycerides (TG) were evaluated by routine methods. Fructosamine (FR) was measured by the nitroblue tetrazolium (NBT) colorimetric test. An elevated level of lipid peroxides (P < 0.001) was observed in the plasma of diabetic patients (4.51 +/- 1.29 nmol/ml) as compared to normal subjects (3.54 +/- 1.00 nmol/ml). Lipid peroxides did not correlate with the FR levels, nor with FBG, TC and TG. These results show an increase of LPO in type 2 normolipidemic diabetic patients. Probably the mechanism for higher lipid peroxide levels in diabetes is multifactorial. Our study supports the hypothesis of a role of oxidative stress in diabetes independently of the lipid serum content.

Aged↗
PubMed1997

[Dermatitis artefacta].

We report a case of a 29-year-old man presenting skin ulcerations on both sides of the mandible. The diagnosis of dermatitis artefacta was based on the morphology and evolution of the lesions, on the patient's borderline personality, on the objects found in his possession, and a later admission of having an involvement in the aggravation of the lesions.

Adult↗
PubMed1997

[Effect of silibinin on oxidative damage of blood constituents].

Silibinin (SDH) is a flavonoid with ascertained hepatoprotective effects, which have been partially attributed to its antioxidant properties. Oxidation of blood constituents could have a role in atherogenesis and interfere with the rheologic properties of the blood. In this study we investigated, whether SDH could protect some blood constituents against oxidative modification. In human plasma we measured TBARS and fluorescence generation as indicators of copper or azobis amidinopropane hydrochloride (AAPH) at 760 mm Hg PO2-induced lipid peroxidation. SDH at 50 microM inhibited copper-induced TBARS formation by 25% and fluorescence by 47%. SDH also inhibited AAPH-induced lipid peroxidation, but at 175 microM concentration only. Oxidative modification of albumine was evaluated by fluorescence generation. SDH at 50 microM inhibited copper/hydrogen peroxide fluorescence generation by 54% and at 2.5 microM it inhibited EDTA-Fe (II)/hydrogen peroxide fluorescence generation by 31%. The protection of albumin by SDH was confirmed by SDS-PAGE electrophoresis. Copper-induced red-cell lipid peroxidation was evaluated by TBARS formation. SDH at 250 microM inhibited copper-induced lipid peroxidation and hemolysis by 45% and 94%, respectively. SDH also inhibited hemolysis in red-cell suspensions exposed to hydrogen peroxide, but not lipid peroxidation. Our results show that SDH may protect blood constituents from oxidative damage.

Blood↗
PubMed1997

[Glycosylation and lipid peroxidation in skin and in plasma in diabetic patients].

Glycation and free radical reactions may play a role in complications of diabetes. Vascular complications, as a consequence of atherosclerosis, are the main causes of morbidity and mortality in diabetes. The aim of this work was to study glycation and lipid peroxidation (LPO) in plasma and skin of type 2 diabetic patients. The levels of advanced glycation endproducts (AGEs) in skin collagens are considered as the sum of accumulated glycation over time. We studied 20 subjects with type 2 diabetes and 20 controls. Glycated proteins were quantified in skin and plasma by affinity chromatography in aminophenyl boronate gels. AGEs were determined on skin collagen by fluorimetry. LPO was evaluated by fluorimetry measuring TBARS in the skin and plasma. Skin collagen-linked fluorescence (CLF) was higher in diabetics (p < 0.01). CLF in diabetics with retinopathy was higher than that of diabetics without retinopathy (p < 0.02). There was a positive correlation between duration of diabetes and skin CLF (p < 0.01). TBARS were higher in skin (p < 0.01) and plasma (p < 0.001) of diabetic patients. We did not find any correlation between CLF and TBARS. This is not surprising taking into account the complexity and multifactorial aspects involved in LPO, while in glycation the main determinant factor is hyperglycemia.

Aged↗
PubMed1996

Different effects of thiol and nonthiol ace inhibitors on copper-induced lipid and protein oxidative modification.

Differences among angiotensin-converting enzyme inhibitors (ACEI) in scavenging reactive oxygen species were described and mainly attributed to the presence or absence of a thiol group. Plasma constituents and red cells are known targets for oxidative damage. Transition metals, like copper, are well known catalizers of free radical generation. In the present study we compared the abilities of captopril (a thiol ACEI), enalaprilat, and lisinopril (two nonthiol ACEI) for inhibiting copper-induced thiobarbituric acid reactive substances (TBARS) formation and fluorescence generation in whole human plasma and low-density lipoprotein. The effects of those ACEI on copper/hydrogen peroxide-induced fluorescence development and electrophoretic mobility modification in albumin and on copper-induced TBARS formation and hemolysis in human red cells were also compared. Captopril was more effective than the two nonthiol ACEI in inhibiting plasma and LDL lipid peroxidation, but it was ineffective in inhibiting the albumin oxidative modification that was moderately inhibited by enalaprilat and lisinopril. On the contrary, the inhibitory effects of the three ACEI on copper-induced lipid peroxidation and hemolysis in red cell suspensions were more uniform. This as yet unreported red cell protective effect may deserve pharmacological evaluation. Our results show that captopril is a more effective antioxidant than the nonthiol ACEI in some systems. However, the nonthiol ACEI also have the ability to partially protect some targets against oxidative damage. These observations suggest that the presence of a thiol group in the ACEI structure is not the only determinant for the antioxidant properties.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Hyaluronic acid in progressive systemic sclerosis.

BACKGROUND: The glycosaminoglycans metabolism is disturbed in progressive systemic sclerosis (PSS). Serum hyaluronic acid (HA) is elevated in this disease. OBJECTIVE: This study was conducted to determine the HA plasma concentrations of patients with PSS according to the different stages of the disease. METHODS: We studied 48 patients divided into three subgroups: subgroup 1 (n = 10), with skin compromise without evidence of other organ involvement; subgroup 2 (n = 21), with skin and esophagus involvement; subgroup 3 (n = 17), with skin, lung and other internal organ involvement. A radiometric assay was performed for quantification of HA. RESULTS: Our results confirm the increase in plasma HA in patients with PSS. They also suggest that lung involvement is the main feature responsible for high plasma concentrations of HA. The plasma HA levels were elevated in patients compared to normals (p <0.001). Significant differences were observed between subgroups 1 and 3 (p <0.01) and between subgroups 2 and 3 (p <0.01). A positive correlation between disease severity scores and plasma HA values was observed (p <0.01). CONCLUSION: An important elevation of HA plasma levels could be a serologic marker of disease severity, progression and degree of visceral involvement.

Adult↗
PubMed1995

[Potential antioxidative effects of pentoxifylline].

Pentoxifylline (PTX) is a methylxanthine derivative with hemorrheologic properties. PTX decreases neutrophil degranulation and tumor necrosis factor production. We investigated the properties of the drug as a hydroxyl radical scavenger. The aim of this study was to assess the ability of PTX to inhibit visible fluoroescence generation in albumin incubated with 50 microM cupric chloride and 880 microM hydrogen peroxide for 3 h at 37 degrees C. PTX inhibited visible fluorescence generation (ex 360, em 454 nm) by 11% at 50 microM, 13% at 100 microM and 22% at 200 microM. In conclusion, PTX inhibited fluorescence generation in proteins induced by copper/hydrogen peroxide and has potential beneficial effects by protecting proteins against oxidative damage by reactive oxygen species.

Albumins↗
PubMed1995

[Lipid peroxidation, production of PGE2 and cellular mortality induced by UV in cultured human skin fibroblasts].

UV irradiation induces lipid peroxidation (LPO) and cell damage. The aim of the present work was the study of UVB radiation effects on cultured human skin fibroblasts, concerning LPO, prostaglandine E2 (PGE2) formation and cell viability. The cells were exposed to 50, 100, and 150 mJ/cm2 of UVB irradiation. Cellular TBARS and supernatant fluorescent substances were measured spectrofluorimetrically. PGE2 was measured using an immunoenzymatic method. Cell viability was evaluated by the MTT test. All determinations were done after a 2 h incubation period post-irradiation. TBARS were increased for all doses of irradiation (p < 0.001). Fluorescent substances differed from controls at 50 mJ/cm2 (p < 0.001). UVB at 100 and 150 mJ/cm2 decreased cellular viability (p < 0.001). An increase of PGE2 was observed with UVB at 150 mJ/cm2 (p < 0.001). These results confirm the occurrence of LPO and cytotoxicity after UV irradiation; on the other hand, this study showed the formation of PGE2 induced by UV light on cultured human skin fibroblasts. We propose a relationship between these phenomena.

Cell Death↗
PubMed1992

[Neurologic manifestations of Behçet disease. Review of the caseload of the Neurology and Dermatology services at the Santa Maria Hospital].

Neurological involvement in a series of patients with Behçet's disease, evaluated at the Departments of Neurology and Dermatology, St. Maria Hospital is reported. Meningoencephalytic or encephalytic were the most common clinical forms, while headache, cerebellar and pyramidal signs were the most prevalent symptoms/signs. On follow-up (range 2-13 years) the majority of the patients had either a progressive or a remitting-progressive course. Magnetic ressonance imaging was the most valuable method of detecting central nervous system lesions.

Adult↗
PubMed1991

Sensitivity to thimerosal and photosensitivity to piroxicam.

17 patients allergic to thimerosal, with no previous history of photosensitivity or piroxicam ingestion, 2 patients with piroxicam-induced photosensitivity, and 10 controls were patch or photopatch tested, with 1 or more of the following: thimerosal, thiosalicylic acid, irradiated and non-irradiated solutions of piroxicam alone, L-cysteine alone and piroxicam plus L-cysteine, and piroxicam in petrolatum., The results of the tests supported the hypothesis that there are cross-reactions between thiosalicylic acid and prioxicam, a photosensitizer. The mechanism of the cross-reactions may involve photoproducts of piroxicam and L-cysteine, as patients allergic to thiosalicylic acid, who have positive photopatch tests to piroxicam, also had positive patch tests to the irradiated solution of piroxicam plus L-cysteine.

Adult↗