Effect of growth factors and steroid hormones on heme oxygenase and cyclin D1 expression in primary astroglial cell cultures.

Astrocyte activity may be modulated by steroid hormones and GFs. This study investigates the interaction between glucocorticoids or estrogens and GFs on the expression of heme oxygenase-1 (HO-1) and cyclin D1 in astrocyte cultures at 14 days treated for 48 or 60 hr with dexamethasone (DEX) or 48 hr with 17ß-estradiol (E2) alone or with GFs added only in the last 12 or 24 hr. Twelve- or twenty-four-hour epidermal growth factor (EGF) treatment significantly enhanced HO-1 expression in astrocyte cultures pretreated for 48 hr with DEX. A highly significant increase in HO-1 expression was obtained after the last-12-hr EGF treatment in 48-hr E2-pretreated astrocyte cultures; this enhancement was particularly significant in 48-hr E2-pretreated cultures as well as in the last-12-hr insulin-treated ones pretreated for 48 hr with E2. Sixty-hour DEX-alone pretreatment as well as the last-12-hr EGF treatment in 60-hr DEX-pretreated astrocyte cultures showed a significant increase of cyclin D1 expression. A significant decrease of cyclin D1 expression in the last-12-hr insulin-like growth factor-I (IGF-1)-treated cultures pretreated for 60 hr with DEX was observed. A highly significant enhancement in cyclin D1 expression in 14 days in vitro astrocyte cultures pretreated with E2 alone for 48 hr and treated in the last 12 hr with IGF-1 in 48-hr E2-pretreated cultures was found. Finally, the data highlight an interactive dialogue between the growth factors and glucocorticoids or estrogens during the maturation of astroglial cells in culture that may control the HO-1 and cyclin D1 expression as well as proliferating astroglial cells during the cell cycle.

The critical role of didodecyldimethylammonium bromide on physico-chemical, technological and biological properties of NLC.

Exploiting the experimental factorial design and the potentiality of Turbiscan AG Station, we developed and characterized unmodified and DDAB-coated NLC prepared by a low energy organic solvent free phase inversion temperature technique. A 22 full factorial experimental design was developed in order to study the effects of two independent variables (DDAB and ferulic acid) and their interaction on mean particle size and zeta potential values. The factorial planning was validated by ANOVA analysis; the correspondence between the predicted values of size and zeta and those measured experimentally confirmed the validity of the design and the equation applied for its resolution. The DDAB-coated NLC were significantly affected in their physico-chemical properties by the presence of DDAB, as showed by the results of the experimental design. The coated NLC showed higher physical stability with no particles aggregation compared to the unmodified NLC, as demonstrated by Turbiscan(®) AGS measurements. X-ray diffraction, Raman spectroscopy and Cryo-TEM images allowed us to assert that DDAB plays a critical role in increasing the lipids structural order with a consequent enhancement of the NLC physical stability. Furthermore, the results of the in vitro biological studies allow the revisiting of the role of DDAB to the benefit of glioblastoma treatment, due to its efficacy in increasing the NLC uptake and reducing the viability of human glioblastoma cancer cells (U87MG).

Cholinergic precursors modulate the expression of heme oxigenase-1, p21 during astroglial cell proliferation and differentiation in culture.

Heme oxygenase-1 (HO-1) plays a crucial role in oxidative stress processes, apoptosis and cell differentiation. Further, some proteins related to cell cycle including cyclins and p21 are important markers of astrocyte cultures. Aim of investigation was to study the effects of cholinergic precursors (choline, CDP-choline, Acetylcholine and α-Glyceril-Phosphorylcholine) on HO-1 and p21 expression during astroglial cell proliferation and differentiation in primary cultures at 14 and 35 days in vitro (DIV) treated for 24 h with choline metabolites. Our results showed a slight reduction of HO-1 expression (data not statistical significant) in astroglial cell cultures treated with CDP-choline at 14 DIV and 35 DIV. On the contrary, ACh and choline induced a significant increase of HO-1 expression in 14 DIV astrocyte cultures. Surprisingly, choline and ACh dramatically reduced HO-1 expression at 35 DIV. A slight decrease not statistical significant was detectable for α-GPC at 14 DIV and particularly significant at 35 DIV. Data concerning p21 expression, a well known protein inhibiting cell cycle, evidenced a significant increase at 14 and 35 DIV after α-GPC treatment. CDP-choline treatment caused a high increase of p21 expression in 14 DIV astrocyte cultures, but no modification at 35 DIV. Instead, ACh treatment induced a marked increment of p21 expression at 35 DIV. Our data suggest that cholinergic precursors modulate HO-1 and p21 expression during astroglial cell proliferation and differentiation in culture and could be considered a tool to study the induced effects of ischemia and hypoxia diseases in some in vitro models to prevent and reduce its effects after treatment with cholinergic drugs.

Sonographic examination of epiaortic vessels in patients with peripheral vertigo.

INTRODUCTION: To evaluate the utility of echo-color-Doppler ultrasonography (CDU) of extracranial brain-supplying vessels in patients with peripheral vertigo of unknown origin. MATERIALS AND METHODS: One-hundred-fifty-six patients (study group; 42 male and 114 female; mean age 61.86 ± 14.14) and 161 patients (control group; 80 male and 81 female; mean age 62.31 ± 13.69) were prospectively evaluated with CDU of extracranial brain-supplying vessels. Plaques in common and/or internal carotid artery (CA), arterial wall intima-media thickness (IMT) of common CA and peak systolic velocity (PSV) and resistive index (RI) of vertebral arteries (VA) were evaluated. Parametric (t-test) and non-parametric (Mann-Whitney U-test and Kolmogorov-Smirnov test) tests were applied. Logistic regression analysis was performed to provide odds ratio indicating the magnitude of risk of vertigo. Independent variables consisting of characteristics (age, sex), vascular risk factors (hypercholesterolemia, diabetes, hypertension) and CDU variables (IMT, plaque, PSV and RI of VA) were considered. RESULTS: Plaques were found in 31 (19.8%) patients of study group and in 43 (26.7%) patients of control group. IMT > 1 mm was found in 98 (62.8%) patients of study group and in 125 (77.6%) patients of control group.Statistical tests, applied to PSV and RI, showed no significant difference (p-value >0.05). At logistic regression analysis, vertigo was associated with age, sex, hypercholesterolemia, diabetes, hypertension and IMT (p < .01) while plaque, PSV and RI of VA were not significant factors (p > .05). DISCUSSION: IMT is the only CDU variable significantly associated with vertigo, especially in the lower age-classes (35-45 and 45-55) of study group.

Are pancreatic calcifications specific for the diagnosis of chronic pancreatitis? A multidetector-row CT analysis.

AIM: To retrospectively establish the most frequently encountered diagnoses in patients with pancreatic calcifications and to investigate whether the association of certain findings could be helpful for diagnosis. MATERIALS AND METHODS: One hundred and three patients were included in the study. The location and distribution of calcifications; presence, nature, and enhancement pattern of pancreatic lesions; pancreatic atrophy and ductal dilatation were recorded. Differences between patients with chronic pancreatitis and patients with other entities were compared by using Fisher's exact test. RESULTS: Patients had chronic pancreatitis (n=70), neuroendocrine tumours (n=14), intraductal papillary mucinous neoplasm (n=11), pancreatic adenocarcinoma (n=4), serous cystadenoma (n=4). Four CT findings had a specificity of over 60% for the diagnosis of chronic pancreatitis: parenchymal calcifications, intraductal calcifications, parenchymal atrophy, and cystic lesions. When at least two of these four criteria were used in combination, 54 of 70 (77%) patients with chronic pancreatitis could be identified, but only 17 of 33 (51%) patients with other diseases. When at least three of these four criteria were present, a specificity of 79% for the diagnosis of chronic pancreatitis was achieved. CONCLUSION: Certain findings are noted more often in chronic pancreatitis than in other pancreatic diseases. The presence of a combination of CT findings can suggest chronic pancreatitis and be helpful in diagnosis.

Effect of choline-containing phospholipids on transglutaminase activity in primary astroglial cell cultures.

The aim of the present investigation was to study the effects of choline and choline-containing phospholipids CDP-choline (CDPC) and L-alpha-glyceryl-phosphorylcholine (AGPC) on transglutaminase (TG) activity and expression in primary astrocyte cultures. TG is an important Ca(2+)-dependent protein that represents a normal constituent of nervous systems during fetal stages of development, playing a role in cell signal transduction, differentiation, and apoptosis. Confocal laser scanning microscopy (CLSM) analysis showed an increase of TG activity in astrocyte cultures treated with choline, CDPC, or AGPC at 0.1 microM or 1 microM concentrations. Comparatively, AGPC induced the most conspicuous effects enhancing monodansyl-cadaverine fluorescence both in cytosol and in nuclei, supporting the evidence of the important role played by AGPC throughout differentiation processes tightly correlated to nucleus-cytosol cross- talk during astroglial cells proliferation and development. Western blot analysis showed that in 24h 1 microM AGPC and choline-treated astrocytes increased TG-2, whereas no effect was observed in 24h 1 microM CDP-choline treated astrocytes. Our data suggest a crucial role of choline precursors during different stages of astroglial cell proliferation and differentiation in cultures.

Effect of acetylcholine precursors on proliferation and differentiation of astroglial cells in primary cultures.

Effects of acetylcholine and of the cholinergic precursors choline, cytidine 5'-diphosphocholine (CDP-choline) and alpha-glyceryl-phosphorylcholine (alpha-GPC) on transglutaminase (TG) and cyclin D1 expression were studied in primary astrocyte cultures by confocal laser microscopy (CLSM) with monodansyl-cadaverine uptake as a marker of enzyme activity and by immunochemistry (Western blotting). CLSM analysis showed an increased cytofluorescence in 0.1 microM choline-treated astrocytes. Treatment with CDP-choline dose-dependently increased TG. A total of 1 microM CDP-choline exposure in 14 days in vitro (DIV) astrocyte cultures increased cytofluorescence. A total of 1 microM alpha-GPC 24 h-treated cultures revealed increased cytofluorescence both in cytosol and nuclei. Western blot analysis showed an increased TG expression in cultures exposed for 24 h to 1 microM choline or alpha-GPC, whereas in 24 h 1 microM CDP-choline and acetylcholine-treated astrocytes TG expression was unaffected. Treatment with 1 microM acetylcholine reduced TG expression at 21 DIV. In cultures at 14 and 35 DIV cholinergic precursor treatment for 24 h induced a marked down-regulation of cyclin D1 expression, with reduced cyclin D1 expression in 1 microM alpha-GPC treated astrocytes. Our data suggest a role of cholinergic precursors investigated independent from acetylcholine on maturation and differentiation of astroglial cells in vitro, rather than on their growth, proliferation and development in culture.

Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures.

Type-2 transglutaminase (TG-2) is a multifunctional enzyme involved in the regulation of cell differentiation and survival that recently has been shown to play an emerging role in astrocytes, where it is involved in both proliferation and differentiation processes. Growth factors (GFs) such as EGF, basic fibroblast growth factor, insulin-like growth factor-I (IGF-I), and insulin (INS) are trophic and mitogenic peptides that participate in neuron-glia interactions and stimulate neuronal and astroglial proliferation and differentiation. Steroid hormones such as glucocorticoids and estrogens also play a pivotal role in neuronal and astroglial proliferation and differentiation and are key hormones in neurodegenerative and neuroprotective processes. We investigated the effects of the interaction of GFs with dexamethasone (DEX) or 17beta-estradiol (E(2)) on TG-2 activity and their expression in cultured astrocytes. We observed a significant increase in TG-2 activity and expression in astroglial cells treated for 24 hr with IGF-I, EGF, or INS. Priming of the cells with DEX or E(2), for 48 hr also led to an increase in TG-2 levels. When growth factors were present in the last 24 hr of the steroid treatment, a reduction in TG-2 expression and activity and a different subcellular TG-2 distribution were found. Our data indicate that steroid hormone-GF interaction may play an important role in astroglial function. The effect on TG-2 could be part of the regulation of intracellular pathways associated with the astrocyte response observed in physiological conditions and, possibly, also in neuropathological diseases.

Evaluation of cell tolerability of a series of lipoamino acids using biological membranes and a biomembrane model.

The interaction of a series of amphiphilic 2-alkyl aminoacids (lipoamino acids, LAAs) with different cell cultures and biomembrane models was investigated. LAAs can be useful promoieties to modify the physico-chemical properties of many drugs, and in particular their lipophilicity. Tests were performed in vitro on mammalian cells (murine astrocytes) and human red blood cells (haemolysis), and in vivo on rabbit eye as alternative models to assess the tolerability or the potential damaging effects of these compounds on different biological systems. The mode of interaction of LAAs with pure phospholipid multilamellar liposomes, taken as a biomembrane model, was also analysed by differential scanning calorimetry experiments. Different tolerability/toxicity patterns were obtained in the various models; in particular, the most lipophilic terms of the series, methyl 2-aminohexadecanoate (LAA16), displayed haemolytic activity and toxicity for mouse astrocyte cultures. A specific assay confirmed that LAA16 acted at level of cell membranes, while neither any damaging effects on nucleus or apoptotic induction were observed. The shorter-chain LAAs and the tetradecyl homologue (LAA14) showed the best compatibility with the various cell models.

Heterogeneous delayed enhancement of hepatic parenchyma after intravenous infusion of sonographic contrast agent: a new hypothesis.

PURPOSE: The aim of this paper was to report a heterogeneous late-phase hepatic enhancement pattern observed after administration of a sonographic contrast agent and to present an aetiological hypothesis for the phenomenon. MATERIALS AND METHODS: A total of 1,729 (1,012 women and 717 men; age range 28-82; mean age 51) patients underwent contrast-enhanced sonography of the liver. The examination was performed with a low mechanical index (MI <0.09) after injection of sulphur-hexafluoride-filled microbubbles, using different sonographic equipment and different contrast-specific algorithms. RESULTS: Heterogeneous delayed liver enhancement was observed in six patients in the late phase (180 s), with the presence of multiple, partially confluent, hyperechoic areas peripheral to the portal vessels. The pattern appeared spontaneously between 1 and 4 h after the examination and was associated with the presence of an anomalous echogenicity in the superior mesenteric vein. No patient experienced adverse reactions. CONCLUSIONS: The phenomenon of heterogeneous hepatic enhancement may be related to gas from the intestinal microcirculation being transported to via the enteroportal circulation and becoming trapped in the hepatic sinusoids.

Effects of cadmium exposure on testis apoptosis in the marine teleost Gobius niger.

It is known that heavy metals can accumulate in tissues during aquatic organism growth (bioaccumulation) and often biomagnify up the food chain interfering with the health and reproduction of both wildlife and humans. Recently, cadmium (Cd) was included in the endocrine disruptors list, exerting its effect on gametes quality and reproductive functions; in addition, its role as apoptotic factor was evidenced in different cell types and tissues. In the present study, the effects of two different Cd doses on testis and liver of the black goby Gobius niger were analyzed. Cd concentration in the water and its uptake by the gills were measured by differential pulse anodic stripping voltammetry. Toxic, apoptotic, and stressor Cd effects were analyzed using metallothionein (MTT), caspase 3 and heath shock protein 70 (HSP70), respectively, as bioindicators. The results of the present study suggested that, in the gills, the saturation of all specific metal sites was reached only with the highest Cd dose exposure. Either testis and liver showed an increase of MTT gene expression and protein synthesis in addition to HSP70 gene expression, related with Cd concentration in the water indicating that both tissues were affected by Cd exposure. In conclusion, the present study, not only shows the toxic effect of Cd on hepatic tissue, but also indicates its potency as apoptotic factor in the testis. This is supported by the increase of caspase 3 gene expression and the presence of its active form in testis of exposed fish.

Glutamate-evoked redox state alterations are involved in tissue transglutaminase upregulation in primary astrocyte cultures.

The aim of this study was to evaluate the involvement of oxidative stress in glutamate-evoked transglutaminase (TGase) upregulation in astrocyte cultures (14 DIV). A 24 h exposure to glutamate caused a dose-dependent depletion of glutathione intracellular content and increased the ROS production in cell cultures. These effects were receptor-mediated, as demonstrated by inhibition with GYKI 52466. The pre-incubation with glutathione ethyl ester or cysteamine recovered oxidative status and was effective in significantly reducing glutamate-increased tissue TGase. These data suggest that tissue TGase upregulation may be part of a biochemical response to oxidative stress induced by a prolonged exposure of astrocyte cultures to glutamate.

Excitotoxic and post-ischemic neurodegeneration: Involvement of transglutaminases.

Neurodegeneration induced by excitotoxicity is a common feature in various neurological disorders. This pathological condition is caused by prolonged stimulation of glutamate receptor subtypes, followed by both intracellular Ca2+ overload and activation of specific genes, resulting in synthesis of enzymes involved in cell stress response. Using experimental in vitro models of excitotoxicity, we demonstrated that glutamate exposure up-regulated tissue transglutaminase in primary cultures of both cerebellar granule cells and astrocytes. These changes were consequent to receptor-mediated Ca2+ influx, as demonstrated by the inhibition with selective antagonists, MK-801 and GYKI 52466. Early increases in different transglutaminase isoforms were also observed in global cerebral ischemia, which closely resembles neuronal damage caused by NMDA receptor activation. These findings agree with a postulated role for transglutaminases in molecular mechanisms of several neurodegenerative diseases. Indeed, increased cross-linking reactions could be of pathologic relevance, as part of biochemical changes observed in neurological disorders.

Cystamine inhibits transglutaminase and caspase-3 cleavage in glutamate-exposed astroglial cells.

Although the precise role of transglutaminase in cell death is unknown, several findings demonstrate that tissue transglutaminase selectively accumulates in cells undergoing apoptosis both in vivo and in vitro. Calcium-dependent transglutaminase reactions are also implicated in several neurodegenerative diseases, including alterations in the release of excitatory amino acids. One prevalent theme in cell damage induced by excitotoxic stimuli in different regions of the CNS is that apoptosis may be executed by intracellular caspase proteases. Furthermore, the presence of functional ion channel-gated receptors in glial cells suggests that also astrocytes can be susceptible to glutamate's toxic effects. In this study, we demonstrated that prolonged exposure to glutamate (100 microM) of cultured astrocytes caused an increase in the expression of tissue transglutaminase (tTG). This effect was prevented by preincubation with GYKI 52466, an antagonist of AMPA/KA receptors. Glutamate exposure also promoted an increase in caspase-3 compared with control cultures. Confocal laser microscopy analysis demonstrated the presence of activated caspase-3 in the cytoplasm as well as in the nucleus. The inhibition of TG-catalyzed reactions by cystamine (1 mM) blocked the activation pathway of caspase-3, with an evident reduction of enzyme cleavage. These results suggest that glutamate increased both TG and caspase-3 in astroglial cells early in the excitotoxin-induced events.

[Locoregional chemotherapy of locally advanced breast cancer in a pre-treated patient: case report]. / Chemioterapia locoregionale nel carcinoma mammario localmente avanzato in paziente pre-trattata: case report.

We report of the use of intra-arterial chemotherapy in one case of locally advanced breast cancer, that had been systemically pre-treated. Locoregional chemotherapy was delivered via percutaneous access. The catheter tip was placed into the subclavian artery and into origin of the internal mammary artery; it was removed after every cycle of treatment. The schedule of chemotherapy was: epirubicin 30 mg/m2, mitomycin 7 mg/m2 and 5 fluouracil 1000 mg. Three cycles were administered, and the treatment was well tolerated. The patient responded to intra-arterial chemotherapy, and she subsequently underwent complete surgical resection. Intra-arterial chemotherapy for breast cancer in an uncommon approach to the treatment of locally advanced disease. Nevertheless, in selected cases, it could be a more effective therapeutic option for patients with systemic chemotherapy-resistant disease.

Glutamate-induced increases in transglutaminase activity in primary cultures of astroglial cells.

Glutamate exposure of astroglial cells caused ligand-gated channel receptor activation, associated with excitotoxic cell response. We investigated the effects of 24 h glutamate exposure on transglutaminase in astrocytes primary cultures at 7, 14, and 21 days in vitro (DIV). Increases in enzyme activity were observed as a function of cell differentiation stage in glutamate-treated cultures. These effects were significantly reduced when GYKI 52466, an AMPA/KA receptors inhibitor, was added to the culture medium prior to incubation with glutamate. Microscopy observation on transglutaminase-mediated, fluorescent dansylcadaverine incorporation in living cells was consistent with these results. Western blotting analysis with monoclonal antibody showed that glutamate also up-regulated tissue transglutaminase expression, which reached the highest values in 14 DIV cultures. Confocal laser scanning microscopy analysis of immunostained astroglial cells showed a mainly cytoplasmic localisation of the enzyme both in control and treated cultures; nevertheless, counterstaining with the nuclear dye acridine orange demonstrated the presence of tissue transglutaminase also into the nucleus of glutamate-exposed and 21 DIV cells. The increases in enzyme expression and localisation in the nucleus of glutamate-treated astroglial cells may be part of biochemical alterations induced by excitotoxic stimulus.

Immunocytochemical and RT-PCR analysis of connexin36 in cultures of mammalian glial cells.

The expression of connexin36 (Cx36) was studied in primary cultures of rat brain glial cells: mature astrocytes, ameboid and ramified microglia and immature oligodendrocytes (at middle period of myelinogenesis). The data from these cells were compared with those obtained from cultures of neocortical and hypothalamic neurons. mRNA encoding Cx36 was investigated by RT-PCR, the Cx36 protein by immunocytochemistry using a polyclonal antibody against Cx36 in cells characterized by antibodies specific for the single cell types. The Cx36 was found in oligodendrocytes, both ameboid and ramified microglial cells and in neurons. Astrocytes showed no detectable expression of the Cx36. The expression of Cx36 in oligodendrocytes and microglial cells suggests an involvement of the direct cell-cell communication channels formed by Cx36 in myelin formation and in brain development, damage and repair processes.

DNA damage in astrocytes exposed to fumonisin B1.

Fumonisins are a group of toxic metabolites mainly produced by Fusarium moniliforme and Fusarium proliferatum, fungi that commonly occur on corn throughout the world. Fumonisin B1 (FB1), structurally resembling sphingoid bases, is an inhibitor of ceramide synthase, a key enzyme involved in de novo sphingolipid biosynthesis and in the reacylation of free sphingoid bases derived from sphingolipid turnover. This inhibitory effect leads to accumulation of free sphinganine (SA) and sphingosine (SO), inducing cell death. However, little is known on the down stream effectors activated by these sphingolipids in the cell death signaling pathway. We exposed rat astrocytes to FB1 with the aim of evaluating the involvement of oxygen free radicals and of some other biochemical pathways such as caspase-3 activity and DNA damage. Our results indicate that FB1 treatment (48, 72 h and 6 days in vitro, DIV, and 10, 50, 100 microM) does not affect cell viability. Conversely, after 72 h of treatment, FB1 (50 and 100 microM) induced DNA damage and an enhancement of caspase-3 activity compared to controls. In addition, FB1 increased the expression of HSP70 at 10 and 50 microM at 48, 72 h, and 6 DIV of treatment. We conclude that DNA damage of apoptotic type in rat astrocytes is caused by FB1 and that the genotoxic potential of FB1 has probably been underestimated and should be reconsidered.

Bioflavonoids as antiradicals, antioxidants and DNA cleavage protectors.

Flavonoids have recently aroused considerable interest because of their broad pharmacological activity. In fact, flavonoids have been reported to have antiviral, antiallergic, antiplatelet, anti-inflammatory and antitumoral activities. The pharmacological properties of bioflavonoids have been ascribed both to the concomitant inhibition of enzymes involved in the production of free radicals and to their free-radical scavenging and iron chelating capacity. However the antioxidant capacity of bioflavonoids due to free-radical scavenging and/or to iron chelating is still controversial. In this study, we have investigated the free-radical scavenging capacity of bioflavonoids (rutin, catechin, and naringin). In addition, the effects of these polyphenols on xanthine oxidase activity, spontaneous lipid peroxidation, and DNA cleavage were investigated. The bioflavonoids under examination showed a dose-dependent free-radical scavenging effect, a significant inhibition of xanthine oxidase activity, and an antilipoperoxidative capacity. In addition, they showed a protective effect on DNA cleavage.

L -propionyl-carnitine as superoxide scavenger, antioxidant, and DNA cleavage protector.

L-Propionylcarnitine, a propionyl ester of L-carnitine, increases the intracellular pool of L-carnitine. It exhibits a high affinity for the enzyme carnitine acetyltransferase (CAT) and, thus, is readily converted into propionyl-coenzyme A and free carnitine. It has been reported that L-propionylcarnitine possesses a protective action against heart ischemia-reperfusion injury; however, the antioxidant mechanism is not yet clear. L-Propionylcarnitine might reduce the hydroxyl radical production in the Fenton system, by chelating the iron required for the generation of hydroxyl radicals. To obtain a better insight into the antiradical mechanism of L-propionylcarnitine, the present research analyzed the superoxide scavenging capacity of L-propionylcarnitine and its effect on linoleic acid peroxidation. In addition, the effect of L-propionylcarnitine against DNA cleavage was estimated using pBR322 plasmid. We found that L-propionylcarnitine showed a dose-dependent free-radical scavenging activity. In fact, it was able to scavenge superoxide anion, to inhibit the lipoperoxidation of linoleic acid, and to protect pBR322 DNA from cleavage induced by H2O2 UV-photolysis.