Efficacy of cosmetic products in cellulite reduction: systematic review and meta-analysis.

BACKGROUND: The number of original articles investigating the efficacy of cosmetic products in cellulite reduction increased rapidly in the last decade; however, to our knowledge, no systematic review and meta-analysis has been performed so far. OBJECTIVE: We conducted a systematic review of in vivo studies on humans adopting the PRISMA guidelines. Moreover, we used a meta-analytic approach to estimate the overall effect of cosmetic creams in cellulite treatment from controlled trials with more than 10 patients per arm, using thigh circumference reduction as the outcome measure. METHODS: Medline and Embase were searched up to August 2012 to identify eligible studies. RESULTS: Twenty-one original studies were included in the present systematic review. All studies were clinical trials, most of them recruited women only and 67% had an intra-patient study design. About half of the active cosmetic creams tested only contained one active ingredient among xanthenes, herbals or retinoids. The other studies tested cosmetic creams with more complex formulations and most of them included xanthenes. A total of seven controlled trials satisfied the inclusion criteria for the meta-analysis. The pooled mean difference of thigh circumference reduction between the treated and the controlled group was -0.46 cm (95% confidence intervals, CI: -0.85, -0.08), with significant heterogeneity between studies (P < 0.001). CONCLUSION: This article provides a systematic evaluation of the scientific evidence of the efficacy of cosmetic products in cellulite reduction and supports a moderate efficacy in thigh circumference reduction.

[Significant two-weeks clinical efficacy of an association between Massaciuccoli peat and sodium chloride water of Undulna Thermae measured on gynoid lipodystrophy in a group of overweight female]. / Efficacia significativa del trattamento di due settimane con associazione di torba del Massaciuccoli ed acqua clorurato-sodica delle terme di Undulna sulla lipodi- strofia a localizzazione ginoide in un gruppo di donne sovrappeso.

BACKGROUND: Peloid has been popularly used as an effective base in cosmetic preparations, although its biologically-active materials and mechanisms on skin have not yet been fully determined. An association between Massaciuccoli peat and sodium chloride water of Undulna Thermae was evaluated as a 2-weeks therapy for gynoid lipodystrophy in a group of 30 overweight females (age: 20-50y, BMI: 25-35 kg/m2) by means of evidence based-medicine criteria. METHODS: The modification of the body diameters was the primary end-point, and the variation of skinfold thicknesses, bioimpendance parameters, evaluation of skin elasticity, rated thermal contact to liquid crystals and measurement of subcutaneous fat tissue were the secondary end-points. It was asked, by visual-analog scale, for an opinion to the patients about effectiveness of treatment. RESULTS: At the end of treatment, after 2 weeks, all body diameters significantly decreased in the intervention group (waist circumference: 91.95 +/- 8.94 versus 90.60 +/- 8.90 cm, p < 0.001). Moreover, total body water were significantly reduced in the intervention group (35.05 +/- 3.74 versus 34.38 +/- 3.41 l, p < 0.03). As regards skin elasticity (+5.52%, p < 0.001), significant improvements have been determined; subcutaneous perfusion was also improved and thickness of subcutaneous fat was significantly reduced (thighs delta = -1.3 mm, p < 0.01; abdomen delta = -4.6 mm, p < 0.001). Furthermore, response to the visual-analog scale was positive (7.55 +/- 0.87). CONCLUSIONS: This treatment appears potentially useful in the clinical management of gynoid lipodystrophy in overweight females.

[Efficacy study in vitro: assessment of the properties of resveratrol and resveratrol + N-acetyl-cysteine on proliferation and inhibition of collagen activity]. / Studio d'efficacia in vitro: valutazione dell'influenza de resveratrolo e resveratrolo + N-acetil-cisteina sulla proliferazione cellulare e sull'inibizione della collagenasi.

During and after menopause the skin shows up clearly how the lack of estrogen affects tissues, and menopause can in fact be considered a "multisystemic" disorder of connective tissue. The low menopausal estrogen levels combined with age-related skin changes, accelerating skin aging. This affects both the epidermis and the dermis: fibroblasts not only become fewer, but they produce 30% less collagen, reflecting its metabolic decline. Estrogens act on collagen synthesis by directly stimulating fibroblasts. However, hormone replacement can prevent the postmenopausal loss of collagen--or eliminate it once it has started. The results of the Women's Health Initiative study drastically changed Italian gynecologists' prescribing habits. Natural products with estrogen-like activity are increasingly accepted, since they have good effects on collagen synthesis and/or inhibit collagenase activity, with a reassuring safety profile. This was confirmed by an in vitro study that assessed the tonic-trophic properties of two treatments on cultured skin fibroblasts. Cells were treated with resveratrol either alone or combined with NAC 10-100-1000 µM. There was a dose-related increase in the rate of cell proliferation and in inhibition of collagenase activity.

Branched-chain amino acid supplementation does not enhance athletic performance but affects muscle recovery and the immune system.

Since the 1980's there has been high interest in branched-chain amino acids (BCAA) by sports nutrition scientists. The metabolism of BCAA is involved in some specific biochemical muscle processes and many studies have been carried out to understand whether sports performance can be enhanced by a BCAA supplementation. However, many of these researches have failed to confirm this hypothesis. Thus, in recent years investigators have changed their research target and focused on the effects of BCAA on the muscle protein matrix and the immune system. Data show that BCAA supplementation before and after exercise has beneficial effects for decreasing exercise-induced muscle damage and promoting muscle-protein synthesis. Muscle damage develops delayed onset muscle soreness: a syndrome that occurs 24-48 h after intensive physical activity that can inhibit athletic performance. Other recent works indicate that BCAA supplementation recovers peripheral blood mononuclear cell proliferation in response to mitogens after a long distance intense exercise, as well as plasma glutamine concentration. The BCAA also modifies the pattern of exercise-related cytokine production, leading to a diversion of the lymphocyte immune response towards a Th1 type. According to these findings, it is possible to consider the BCAA as a useful supplement for muscle recovery and immune regulation for sports events.

[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]. / Sperimentazione di un nuovo antiossidante topico a base di Furfuril palmitato nel trattamento delle dermatiti eczematose del bambino e del neonato. Risultati di uno studio clinico multicentrico.

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.

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.

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.

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.

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(-).

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.

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.

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.

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.

Synaptosomal iron-dependent lipid peroxidation inhibition after subarachnoid hemorrhage by lazaroid in vivo treatment.

The production of oxygen-free radicals and their subsequent peroxidative action on membrane unsaturated fatty acids could be enhanced after subarachnoid hemorrhage (SAH). We have studied the effects of the in vivo pharmacological treatment with a lazaroid (U78517F) after experimental SAH, on lipid peroxidative patterns in cortical synaptosomal preparations. U78517F is a lipid-soluble antioxidant with a potent action to inhibit iron-dependent lipid peroxidation. Experimental SAH was induced in anesthetized rats by slow injection of 0.3 mL of autologous arterial blood into cisterna magna. The hemorrhagic animals were treated with 5 mg/kg iv of U78517F immediately after surgical operation. The animals were sacrificed 1 d after the hemorrhage and the thiobarbituric acid reactive material (TBAR) was assayed in basal conditions and after 1, 3, 5, 10, and 20 min of incubation at 37 degrees C with a pro-oxidant mixture on three different rat groups: sham-operated (0.3 mL of mock cerebrospinal fluid (CSF) into cisterna magna), hemorrhagic (0.3 mL of autologous arterial blood into cisterna magna), and hemorrhagic-treated. The hemorrhagic event did not influence the membrane lipoperoxidation levels in basal conditions, whereas peroxidative stimulation in vitro caused significant increases in hemorrhagic animals compared to the sham-operated, and in hemorrhagic-treated animals, the synaptosomal TBARs were similar to controls. The pharmacological treatment showed its effectiveness only following incubations with pro-oxidants; therefore, U78517F seems to be protective for membranes in case of severe lipid peroxidative stress.

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.

Amifostine (WR-2721, Ethyol(TM)) can protect human endothelial but not tumor cells from cisplatin-induced cytotoxicity.

Amifostine (WR-2721, Ethyol(TM)) is a chemo-and radioprotective agent which is increasingly used in clinical practice to minimize antitumor therapy-induced toxicities. The key of this property of amifostine is certainly its selective action in terms of differential protection of normal tissue and not of tumor cells. Using HUVEC cells and three different cancer cell lines (A549 non-small cell lung cancer, DND-1A melanoma and HeLa cervical carcinoma) we provide evidence that amifostine could protect normal, and not cancer cells, from cisplatin (CDDP)-induced cytotoxicity in vitro. Furthermore, low doses of amifostine, easily attainable in vivo, can protect 50% of normal cells in vitro from CDDP-induced cytotoxicity.

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.

Antioxidant enzymatic system and free radicals pathway in two different human cancer cell lines.

Resistance to oxidative damage is an important feature of cancer cells. Cellular anti-radical enzymes, lipid peroxidation, glutathione pathway, capability to produce ROS, and cells' susceptibility to H2O2 and menadione toxicity, were analyzed in DND-1A and HeLa cancer cell lines. SOD and GSHPx activities were higher in DND-1A than in HeLa cells. Lipid peroxidation was the same in both cell lines, while menadione stimulation of ROS production was tenfold higher in HeLa cells. Total and reduced, but not oxidized, glutathione levels, were tenfold smaller in HeLa cells. H2O2 proved fatal to HeLa cells after 12 hours' incubation, while it was ineffective on DND-1A; DND-1A cells were more sensitive to menadione toxicity than HeLa cells. The two lines behaved differently in response to the above treatments. These observations might be important in designing more specific cancer treatments.

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).