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F Marzatico

Publications and source records attributed to F Marzatico.

At least 19 recordsLinked to original sources
PubMed2002

[Experimental survey of a new topical anti-oxidant based on furfuryl palmitate in the treatment of child's and baby's dermatitis with eczema: results from a multicenter clinical investigation].

In this paper we present the preliminary results of a multi-center clinical investigation carried out on a new topical product (Triderm(R) Lenil+) containing Superoxidodismutase (SOD), 18-beta glycyrrethic acid, Vitamin E, alpha bisabolol and a new patented antioxidant molecule, Furfuryl palmitate. These active agents altogether protect skin from cell damages that promote the inflammatory syndrome; their action is furthermore sustained by agents such as phytosphingosine and phytosterols that act to repair the skin barrier. Furfuryl palmitate is an ester with a strong quenching ability towards the singlet oxygene (1O2) and with a high permeability potential through the biological membranes, thanks to its lipophylic formula. Further than being among the main responsible for skin ageing, the 1O2 is involved in the genesis of many topical pathologies such as allergic and irritant dermatitis, atopic dermatitis, inflammation, psoriasis and sunburns. The product has been extensively tested for its effectiveness and skin tolerability on a selected population of 60 children and babies with age ranging from 2 months to 14 years, suffering mainly with atopic dermatitis and irritant dermatitis. The topical use of the product caused a significant improvement of the inflammatory skin conditions, with evident and fast inflammation and eczema reduction in all the investigated pathologies, as shown in the present study. The product has been formulated in order to avoid any sensitisation risk and did not show any relevant side effect. It is particularly suitable in the treatment of pediatric dermatitis with symptoms like eczema, itching, desquamation and xerosis.

Administration, Topical↗
PubMed2001

Prevention of neuronal cell damage induced by oxidative stress in-vitro: effect of different Ginkgo biloba extracts.

The effect of two different Ginkgo biloba extracts (GB1 and GB4) was studied in-vitro on cultured neurons exposed to oxidative stress caused by H2O2(50 micromol L(-1)) and FeSO4(100 micromol L(-1)). Only about 50% of the neurons were still viable at the end of the experiment (8 h) in control conditions, while the two extracts dose dependently increased the number of viable cells, in the concentration range 10-200 microg mL(-1). The two Ginkgo biloba extracts differed in their effect on hydroxyl-radical-scavenging capacity: GB1 and GB4 had an IC50 (50% inhibiting concentration) value of 78 microg mL(-1) and 186 microg mL(-1), respectively. However, both extracts inhibited apoptosis in cortical neurons after oxidative stress in-vitro. These observations make one suppose that different preparations of Ginkgo biloba have quantitatively different actions and outline the importance of the contribution of apoptosis prevention toward their neuroprotective action.

Animals↗
PubMed2000

Reduction of lipid peroxidation in different rat brain areas after cabergoline treatment.

Oxidative stress and mitochondrial damage are involved in Parkinson's disease (PD). Several drugs used for PD treatment have demonstrated antioxidant properties. To evaluate the antioxidant efficacy of cabergoline, an ergot derivative with a long plasma half-life, male Wistar rats were treated with vehicle or with 2.5 mg kg(-1)and 10 mg kg(-1)of the drug three, six, or 10 times at 48-h intervals. Cabergoline decreased basal lipid peroxide levels (LPO) in the hippocampus of rats given 10 mg kg(-1)10 times, and in the striatum of rats given the same dose six or 10 times. Spontaneous LPO was inhibited in the hippocampus of rats given 10 mg kg(-1)10 times. Stimulated LPO was decreased in the striatum of rats given 10 mg kg(-1)six times and in rats given 2.5 and 10 mg kg(-1)10 times. The ability of cabergoline to reduce LPO suggests its anti-lipoperoxidative properties.

Animals↗
PubMed2000

In vitro antioxidant properties of amifostine (WR-2721, Ethyol).

PURPOSE: Amifostine (WR-2721), a phosphorylated aminothiol pro-drug which is an analogue of cysteamine, is a selective cytoprotective agent for normal tissues from the toxicities associated with chemotherapy and irradiation. Despite a growing number of reports strongly supporting amifostine's clinical efficacy, few authors have focused on the biochemical basis of amifostine's antioxidant activity. METHODS: We report on amifostine's free-radical scavenging activity against superoxide (O(2;(-))), hydroxyl (OH(-)) and lipoperoxyl radicals in an in vitro model, using pure chemical systems. Amifostine was dephosphorylated to its active metabolite, WR-1065, by adding 10% non-heat-inactivated serum; different amifostine concentrations (1, 10, 50, 100 microM and 200 microM) and pH conditions (pH 5, 7.4 and 9) were tested. RESULTS: Independent of the concentration, amifostine exhibited no major activity against O(2;(-)) ions, neither did any pH variations in the experimental model provide any scavenger effects of the drug against O(2;(-)) radicals. On the other hand, the protective effect of amifostine against OH(-) radicals was confirmed, yielding an EC(50) of 255 microM at pH 7.4 and 230 microM at pH 5. Finally, amifostine exhibited scavenging activity against spontaneous lipoperoxidation, but no apparent antioxidant effect on iron ascorbate-induced lipoperoxidation. CONCLUSIONS: With this in vitro study, we are able to confirm the scavenging activity of the chemo- and radioprotector amifostine, whose activity seems to be particularly important from a biological point of view, since it is exerted mainly against highly reactive OH(-).

Amifostine↗
PubMed2000

Age and sex differences in human skeletal muscle: role of reactive oxygen species.

Previous studies, conducted on experimental animals, have indicated that reactive oxygen species (ROS) are involved in the aging process. The objective of this work was to study the relationship between oxidative damage and human skeletal muscle aging, measuring the activity of the main antioxidant enzymes superoxide dismutase (total and MnSOD), glutathione peroxidase (GPx) and catalase in the skeletal muscle of men and women in the age groups: young (17-40 years), adult (41-65 years) and aged (66-91 years). We also measured glutathione and glutathione disulfide (GSH and GSSG) levels and the redox index; lipid peroxidation and protein carbonyl content. Total SOD activity was lower in the 66-91 year-old vs. the 17-40 year-old men; MnSOD activity was significantly greater in 66-91 year-old vs. 17-40 year-old women. GPx activity remained unchanged. The activity of catalase was lower in adults than in young men but higher in the aged. We observed no changes in GSH levels and significantly higher GSSG levels only in aged men vs. adult men, and a significant decrease in aged women vs. aged men. The protein carbonyl content increased significantly in the 41-65 and 66-91 year-old vs. the 17-40 year-old men. Finally, young women have lower lipid peroxidation levels than young men. Significantly higher lipid peroxidation levels were observed in aged men vs. both young and adult men, and the same trend was noticed for women. We conclude that oxidative damage may play a crucial role in the decline of functional activity in human skeletal muscle with normal aging in both sexes; and that men appear to be more subject to oxidative stress than women.

Adolescent↗
PubMed1999

Age-dependent changes of antioxidant activities and markers of free radical damage in human skeletal muscle.

This study was conducted in order to provide evidence for the role of reactive oxygen species (ROS) in human skeletal muscle aging. We used human muscle samples obtained from hospitalized patients in an open study with matched pairs of individuals of different ages. The subjects, ranging in age from 17 to 91 years, were grouped as follows: 17-25-, 26-35-, 36-45-, 46-55-, 56-65-, 66-75-, 76-85-, and 86-91-year-old groups. To investigate the relationship between muscle aging and oxidative damage we measured total and Mn-dependent superoxide dismutase (total SOD, MnSOD), glutathione peroxidase (GSHPx), and catalase (CAT) activities; total reduced and oxidized glutathione (GSHtot, GSH, and GSSG) levels; lipid peroxidation (LPO), and protein carbonyl content (PrC). Total SOD activity decreases significantly with age in the 66-75-year-old group, although MnSOD activity increases significantly in the 76-85-year-old group. The activity of the two H2O2 detoxifying enzymes (GSHPx and CAT) did not change with age, as do GSHtot and GSH levels. GSSG levels increased significantly (76-85- and 86-91-year-old groups) with age. We observed a significant increase in LPO levels (66-75- and 76-85-year-old groups), although the PrC content shows a trend of increase without gaining the statistical significance. These results support the idea that ROS play an important role in the human muscle aging process.

Adolescent↗
PubMed1998

Antioxidant enzymatic activities and lipid peroxidation in cultured human chondrocytes from vertebral plate cartilage.

In vitro models based on primary cultured human chondrocytes could be useful to study the ROS-mediated inflammatory processes that seem to involve chondrocytes in vivo. In this work, we studied the enzymatic antioxidative capability of human chondrocytes removed from vertebral plates during micro-discectomy and cultured 18 days, measuring total superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx) activities. We also evaluated in the same cells the amount of malondialdehyde (MDA) in order to verify the effect of the variation of the cellular enzymatic antioxidative capability on the degree of membrane lipid peroxidation. Total SOD activity increased, even if not significantly, between the 12th and the 18th day. A significant variation of GSHPx (P<0.01) and of catalase (P<0.001) activity was observed between the 3rd and the 6th day with no further variation until the 18th day. A significant increase (P<0.001) of lipid peroxidation from the 3rd to the 18th day was also observed. These results seem to indicate that only fresh human cultured chondrocytes are suitable to study, through in vitro models, the in vivo behavior of the antioxidative status of these cells.

Cartilage↗
PubMed1998

Antioxidant status and alpha1-antiproteinase activity in subarachnoid hemorrhage patients.

The antiproteasic activity of alpha1-antitrypsin (alpha1-AT) is reduced in cases of subarachnoid hemorrhage from ruptured intracranial aneurysm and particularly in patients currently smoking; alpha1-AT is very sensitive to oxidant agents. About 50% of physiological anti-oxidant systemic capacity is represented by Vitamin A, E and C. Plasmatic amounts of alpha1-AT, alpha1-AT Collagenase Inhibitory Capacity (CIC) and levels of vitamin A, vitamin E and vitamin C were analyzed in 39 patients, 26 women and 13 men, operated for intracranial aneurysm; 11 patients with unruptured intracranial aneurysm were considered as controls while 28 patients were included within 12 hours from subarachnoid hemorrhage (SAH). Plasmatic levels of vitamin A and vitamin E were significantly lower (p=0.038 and p=0.0158) in patients suffering SAH than in controls, while no statistically significant differences were found in mean plasmatic vitamin C levels. Level of alpha1-AT was not statistically different in controls and in patients with SAH; however, the activity of alpha1-AT, evaluated as CIC, is significantly reduced in patients with SAH (p=0.019). We have observed that systemic plasmatic levels of vitamins did not significantly differ in relation to smoking habit. Vitamin A and E represent an important defensive system against free radicals reactions. Particularly, vitamin E acts as an antioxidant by scavenging free-radicals. A reduced anti-oxidant status might be related to the higher sensibility of alpha1-AT to oxidative reactions and the activity of alpha1-AT is dependent on the antioxidant capacity of liposoluble vitamins. We can speculate that an acute systemic oxidative stress condition might influence the rupture of intracranial aneurysms.

Antioxidants↗
PubMed1998

Oxidative stress in the human brain after subarachnoid hemorrhage.

OBJECT: The aim of this study was to verify the patterns of antioxidant enzymatic activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the human brain after subarachnoid hemorrhage (SAH) to verify whether an "oxidative stress situation" characterizes the brain response to subarachnoid bleeding. METHODS: Forty samples of gyrus rectus or temporal operculum that were obtained during a surgical approach to anterior circulation aneurysms were used for this study. The activity of total SOD, GSH-Px, and the SOD/GSH/Px ratio (which expresses the balance between the production of hydrogen peroxides by dismutation of superoxide radicals and the scavenging potential) were calculated in each case. Twelve samples were obtained from patients who underwent surgery for unruptured aneurysms (control group); 13 samples were obtained during surgical procedures performed within 72 hours of SAH; and 15 samples were obtained during delayed surgical procedures (> 10 days post-SAH). Ten patients presented with clinical deterioration caused by arterial vasospasm. In both SAH groups, the mean total SOD activity was significantly higher than in the control group (p=0.029). The mean activity of GSH-Px did not differ significantly between the SAH and control groups (p=0.731). There was a significant increase in the SOD/GSH-Px ratio in both SAH groups, as compared with controls (p < 0.05). There was a significant correlation between the enzymatic activity and the clinical severity of the hemorrhage, with findings of lower values of SOD and, mainly, of the SOD/GSH-Px ratio in the poor-grade patients. The SOD/GSH-Px ratio was 2.14+/-0.44 in patients who presented with clinical vasospasm and 1.24+/-0.2 in cases without vasospasm. CONCLUSIONS: The results of this study show an imbalance of the antioxidant enzymatic activities in the human brain after SAH. which is linked to the severity of the initial bleeding and possibly modified by the development of arterial vasospasm.

Aneurysm, Ruptured↗
PubMed1997

Superoxide dismutase activity in cisternal cerebrospinal fluid after aneurysmal subarachnoid haemorrhage.

It has been recognised that the level of superoxide dismutase (SOD) significantly increases in CSF as the result of cerebral ischaemic damage. The aim of this study was to correlate the CSF levels of SOD enzymatic activity to the patterns of subarachnoid haemorrhage with regards to ischaemic complications due to vasospasm. A series of 78 patients operated on for intracranial aneurysms was studied; all patients were monitored with serial TCD measurements every second day after SAH. CSF samples were obtained at surgery by cisternal puncture of the subarachnoid cistern nearest to the aneurysm. SOD activity was assayed spectrophotometrically. Mean cisternal CSF level of SOD in 12 control cases (12.99 +/- 2.33 U/ml) is significantly higher (p < 0.01) than in 26 patients operated on between day 1 and 3 from last SAH episode (4.44 +/- 0.7 U/ml) and in 40 patients treated by delayed surgery (7.64 +/- 0.92 U/ml). In 13 patients presenting neurological deterioration related to arterial vasospasm mean cisternal SOD level was 12.23 +/- 1.86 U/ml; in 27 cases without vasospasm mean level was 5.43 +/- 0.7 U/ml (p < 001). The present results suggest that (a) cisternal CSF levels of SOD significantly decreases after SAH, probably in relation to an impaired synthesis in the brain compartment and that (b) a substantial elevation of SOD levels is evident in patients suffering ischaemic complications vasospasm-related. Biochemical events in the brain compartment could influence the expression and release of anti-oxidant enzymes in CSF after SAH.

Cerebral Ventricles↗
PubMed1997

Blood free radical antioxidant enzymes and lipid peroxides following long-distance and lactacidemic performances in highly trained aerobic and sprint athletes.

OBJECTIVE: We have determined the differences of the influence of prolonged exercise or higher intensity lactacidemic exercise, on plasma lipid peroxidation and on erythrocyte antioxidant enzymatic defence system. EXPERIMENTAL DESIGN: We measured plasma indices of lipid peroxidation, conjugated dienes (CD) and malondialdehyde (MDA) and erythrocyte enzymes superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase (CAT). The biochemical evaluations were performed in six healthy control males (C) and twelve athletes: six marathon runners (MR) and six sprint-trained athletes (STA) at rest and after a half-marathon (MR) and a training session of 6 x 150 m (STA). RESULTS: In resting conditions MDA was higher in STA and MR than in C (p < 0.01), while only the MR showed significantly elevated levels of CD (p < 0.05). In STA the enzymatic scavenging capacity showed a significantly higher SOD (p < 0.01) and GSHPx (p < 0.01), while CAT was lower than in controls (p < 0.05). In MR only SOD (p < 0.01) was significantly higher than in C. It increased significantly immediately after half-marathon, while CAT decreased 24 and 48 hours postexercise respectively. In these athletes the lipoperoxidative indices increased in the early postexercise phase, while at 24 and 48 hrs both CD and MDA levels decreased. In STA enzyme activities were not modified by anaerobic performance while CD showed a peak 6 hrs postexercise and the MDA showed a progressive increase until 48 hrs afterwards. CONCLUSIONS: Both strenuous long duration exercise and exhaustive sprint training overwhelm our capacity to detoxify ROS, producing oxidative stress. Thus an adequate supply of antioxidants could be appropriate.

Adult↗
PubMed1996

Oxidative stress after acute and chronic application of beta-amyloid fragment 25-35 in cortical cultures.

The aim of this work was to investigate whether free radical reactions play a role in beta-amyloid neurotoxicity. Rat cortical neurons were exposed acutely (24 h) or chronically (3, 7 days) to beta-amyloid biologically active fragment beta 25-35 (50 microM). In these conditions, where only the longest exposure induced neuronal death, superoxide dismutase activity was increased after acute exposure but no change was detected after chronic treatments, whereas a different pattern was observed for glutathione peroxidase. In the basal condition, there was an eight-fold increase in dichlorofluoroscein, used as peroxide production marker, in neuronal cells after 7 days treatment with beta 25-35. Moreover, the intracellular peroxide production induced by Fe2+/ascorbate stimulation was amplified by beta 25-35, increasingly up to 7 days of exposure, by which time the dichlorofluoroscein-stimulated levels were 33 times higher than in controls. In conclusion, our results show that oxidative stress and free radical production are linked to beta 25-35 exposure and may contribute to neurodegenerative events associated with beta-amyloid deposits in Alzheimer's disease.

Alzheimer Disease↗
PubMed1996

Alpha 1-antitrypsin activity in subarachnoid hemorrhage.

An altered equilibrium of protease/protease-inhibitor factors may be involved in the pathogenesis of aneurysm rupture: alpha 1-antitrypsin (alpha 1-AT) represents the most relevant inhibitor of elastase, a proteolytic enzyme enhancing catabolic processes of collagen metabolism. In the present study we test the hypothesis whether the activity of alpha 1-AT is altered in SAH patients; 5 cases with unruptured intracranial aneurysm and 27 patients with diagnosis of aneurysm SAH were included in the study. Blood samples were obtained immediately at admission. As control samples we consider the 5 cases of unruptured aneurysm, 15 cases of unruptured aortic aneurysms and 10 patients with non-vascular CNS diseases. Measurement of alpha 1-AT level was determined by immunoturbidimetric method. Serum levels of alpha 1-AT are significantly lower in patients admitted within 72 hours after SAH, if compared to patients admitted in a delayed phase. The linear relationship between alpha 1-AT and collagenase inhibitory percentage capacity (CIC) was shown to be different in the 4 subgroups considered, and so were the mean % CIC values in the between-groups comparison, except for unruptured aneurysm vs controls. The alpha 1-AT CIC in patients with SAH is shown to be the lowest when compared to controls and unruptured aneurysms (p = 0.0001).

Collagenases↗
PubMed1995

Oxidative events in neuronal and glial cell-enriched fractions of rat cerebral cortex.

The aim of this work was to investigate how neurons and glial cells separated from rat brain cortex respond to "in vitro" oxidative stress induced by incubation of the cellular fractions in the presence of prooxidant mixtures; in addition, the endogenous enzymatic antioxidant capacity of the purified fractions was investigated. Neuronal and glial cell-enriched fractions were obtained from rat cerebral cortex following passages of the tissue through meshes and centrifugations. The following parameters were evaluated: antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), and glucose-6-phosphate dehydrogenase (G6PDH); lipid peroxidation products (TBARS) prior to (basal) and after (iron-stimulated) incubation with a mixture of iron and ascorbic acid; intracellular production of reactive oxygen species (ROS) using a fluorescent probe, dichlorofluorescin-diacetate, in basal, iron-stimulated, and menadione stimulated conditions. SOD and GSHPx activities showed no significant changes between neurons and glia, whereas CAT and G6PDH activities were found to be significantly lower in glia than in neurons. TBARS levels were significantly lower in the glial fraction than in neurons, both in basal and iron-stimulated conditions. ROS production showed no differences between neurons and glia in both basal and menadione-stimulated conditions. Iron-stimulation produced a marked increase in ROS production, limited to the neuronal fraction, with the glial values being similar to the basal ones. Our conclusion is that glia and neurons isolated from rat cerebral cortex show a similar pattern of the most important antioxidant enzymes and of their basal ROS production, whereas glia is more resistant in "oxidative stress" conditions.

Animals↗
PubMed1994

Experimental subarachnoid hemorrhage: events related to anti-oxidant enzymatic systems and eicosanoid peroxide enhancement.

Experimental and clinical studies have emphasized the role of free radicals in the pathogenesis of vasospasm and neurological dysfunction after subarachnoid hemorrhage (SAH). Increases in both enzymatic (arachidonic acid cascade and eicosanoid peroxide production) and non-enzymatic (thiobarbituric acid reactive substances production) lipid peroxidation were found, pointing out the key role of arachidonic acid cascade in impairing membrane functionality in the post-hemorrhage brain. The aim of this work is to investigate whether a correlation exists between time-dependent modifications of eicosanoid peroxide production ("ex vivo" release of leukotriene C4 = LTC4) and antioxidant enzymatic systems in the brain after experimental subarachnoid hemorrhage in the rat. The release of the LTC4 is significantly enhanced at 1, 6 and 48 hours after SAH induction. Cu-Zn superoxide dismutase (SOD) activity is significantly reduced at 6 and 48 hours after SAH induction; Mn-SOD activity is significantly affected at 1, 6 and 48 hours after the hemorrhage. GSH-Px activity is significantly reduced only in the late phase (48 hours) after SAH. The linear regression of statistical analysis, performed to investigate any possible relationship among time-dependent modifications shows that the "ex vivo" release of LTC4 is significantly related to the decreasing trend of MnSOD activity (p < 0.001). The present results suggest that after SAH, a deficit in endogenous anti-oxidant defenses may play a role in making the brain more susceptible to lipid peroxidative events.

Animals↗
PubMed1994

Changes in non-synaptosomal and synaptosomal mitochondrial membrane-linked enzymatic activities after transient cerebral ischemia.

Non-synaptosomal and synaptosomal mitochondrial membrane-linked enzymatic activities, NADH-cytochrome c reductase rotenone insensitive (marker of the outer membrane) and cytochrome oxidase (marker of the inner membrane), were measured in rat brain hippocampus and striatum immediately after and 1, 4 and 7 days following the induction of complete transient ischemia (15 min) by the four vessel occlusion method. Furthermore citrate synthetase activity was measured with and without Triton X-100 in order to qualitatively evaluate the membrane permeability. Non-synaptosomal mitochondrial membranes showed reduction of both activities only in the late reperfusion phase: NADH-CCRRi decreased in striatal mitochondria after 4-7 days and only after 7 days in the hippocampus. COX activity decreased only in striatal mitochondria 7 days after ischemia. Non-synaptosomal mitochondrial membrane permeability did not show changes. Synaptosomal mitochondria showed a decrease of NADH-CCRRi only at 7 days of reperfusion both in hippocampus and striatum, while COX activity decreased only during ischemia and returned to normal levels in the following days in the two areas considered. In summary, free mitochondria showed insensitiveness to ischemia but they resulted damaged in the late reperfusion phase, while mitochondria from the synaptic terminal showed ischemic damage, partially restored during reperfusion. The striatal mitochondria showed a major susceptibility to ischemia/reperfusion damage, showing changes earlier than the hippocampal ones.

Animals↗