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PubMed1986

Induced precipitation of calcium-oxalate crystals and its prevention in laboratory animals.

Induced precipitation of Ca-oxalate crystals and the possibility of its prevention were studied in dogs. In the first phase of the experiments precipitation of Ca-oxalate crystals in canine renal tubules was induced by intraperitoneal administration of Na-glyoxylate. Preventive medication (lipoic acid, vitamin B1, Milurit), applied in the second phase, resulted in a significant depression of induced precipitation. The successful experiments serve as a basis for clinical research aimed at a preventive medication of recurrent Ca-oxalate stone formation.

Animals↗
PubMed1993

Growth of normal human ovarian surface epithelial cells in reduced-serum and serum-free media.

The human ovarian surface epithelium (OSE) is believed responsible for over 85% of ovarian cancers, yet little is known about the normal biology of these cells. To date, culture of OSE has only been reported in media with high serum supplements. We have developed two media, one with less than 1% of serum (OSEM-1) and the other comprised of highly purified and defined materials (OSEM-2), which allow us to study OSE under relatively defined conditions. By substituting 0.05% of Pedersen's fetuin for 15% fetal bovine serum (FBS) with Medium 199/MCDB105 basal medium, the cell numbers reached 50 to 60% of those in the presence of 15% FBS over 7 days. However, over several weeks, the total number of population doublings achieved were comparable to those in 15% FBS. Addition of insulin, transferrin, ethanolamine, lipoic acid, and phosphatidylcholine to the medium with Pedersen's fetuin (OSEM-1) enhanced growth up to 20% more than in their absence. Supplementation of M199/105 with highly purified (> 99%) fetuin, alpha 2-macroglobulin, and hydrocortisone resulted in a defined medium (OSEM-2) that permitted 1 to 2 doublings/7 days. In addition, cells maintained a more normal, epithelial-like morphology in culture for a longer period in the presence of Pedersen's or purified fetuin than in M199/105/15% FBS, thus increasing the number of morphologically normal cells available for experimentation. Addition of 0.05% Pedersen's fetuin to M199/105 in the presence of 6 to 8% FBS resulted in levels of growth equivalent to those in M199/105/15% FBS alone. We are now able to study the effects of various compounds on the growth and differentiation of OSE under defined conditions, and have reduced the requirement for FBS to produce large numbers of OSE cells.

Cell Count↗
PubMed1999

Potential carcinogenicity of some transition metal ions.

Potential carcinogenicity of some transition metal ions was tested using a direct-current polarography method. The measurements were based on the reduction of tested compounds in an anhydrous solution using alpha-lipoic acid as the detection compound. The potential carcinogenicity was expressed in terms of the parameter tg alpha, which is known to directly correlate with the carcinogenicity of tested compounds. For the metal ions tested, tg alpha was found to decrease in the following sequence: Fe(III) > Pb(II) > V(IV) > Fe(II) > Mn(II) > Cu(II). Zero values of tg alpha were found for Cd(II) and Mn(III).

Animals↗
PubMed2003

Justification for antioxidant preconditioning (or how to protect insulin-mediated actions under oxidative stress).

Insulin resistance is characterized by impaired glucose utilization in the peripheral tissues, accelerated muscle protein degradation, impaired antioxidant defences and extensive cell death. Apparently, both insulin and IGF-1 at physiological concentrations support cell survival by phosphatidylinositol 3 kinase-dependent and independent mechanisms. Postprandial hyperglycemia and hyperinsulinemia are found in insulin resistance, which accompanies the so-called noninsulin dependent diabetes mellitus (diabetes type 2). Evidence also indicates that increased susceptibility of muscle cells and cardiomycoytes to oxidative stress is among the harmful complications of insulin resistance and diabetes. Limited knowledge showing benefits of preconditioning with anti- oxidants (vitamin C, E, a-lipoic acid, N-acetylcysteine) in order to protect insulin action under oxidative stress prompted the author to discuss the theoretical background to this approach. It should be stressed that antioxidant preconditioning is relevant to prevention of both diabetes- and insulin resistance-associated side-effects such as low viability and cell deletion. Furthermore, antioxidant conditioning promises to provide higher efficacy for clinical applications in myoblast transfer therapy and cardiomyoplasty.

Animals↗
PubMed2005

The carbonyl scavengers aminoguanidine and tenilsetam protect against the neurotoxic effects of methylglyoxal.

Advanced glycation end products (AGEs) have been identified in age-related intracellular protein deposits of Alzheimer's disease (amyloid plaques and neurofibrillary tangles) and Parkinson disease (Lewy bodies), suggesting that these protein deposits have been exposed to AGE precursors such as the reactive dicarbonyl compound methylglyoxal. In ageing tissue and under diabetic pseudohypoxia, intracellular methylglyoxal levels rise through an impairment of triosephosphate utilization. Furthermore, methylglyoxal detoxification is impaired when reduced glutathione levels are low, conditions, which have all been described in Alzheimer's disease. However, there is less known about the toxicity of methylglyoxal, particularly about therapeutic strategies to scavenge such dicarbonyl compounds and attenuate their toxicity. In our study, extracellularly applied methylglyoxal was shown to be toxic to human neuroblastoma cells in a dose-dependent manner above concentrations of 150 microM with a LD50 of approximately 1.25 mM. Pre-incubation of methylglyoxal with a variety of carbonyl scavengers such as aminoguanidine or tenilsetam and the thiol antioxidant lipoic acid significantly reduced its toxicity. In summary, carbonyl scavengers might offer a promising therapeutic strategy to reduce the neurotoxicity of reactive carbonyl compounds, providing a potential benefit for patients with age-related neurodegenerative diseases.

Cell Line, Tumor↗
PubMed2003

Antioxidant agents are effective in inducing lymphocyte progression through cell cycle in advanced cancer patients: assessment of the most important laboratory indexes of cachexia and oxidative stress.

This study assessed in a wide population of advanced cancer patients the biological parameters relevant to cancer cachexia, such as serum levels of proinflammatory cytokines (IL-1beta, IL-6, TNFalpha), IL-2, acute-phase proteins (C-reactive protein and fibrinogen), leptin, and relevant to oxidative stress (OS), such as ROS, body antioxidant enzymes GPx and SOD. We also studied the ability of effective antioxidant agents alpha-lipoic acid (ALA), N-acetyl cysteine (NAC), and amifostine (AMI) added into culture to induce lymphocyte progression through the cell cycle, namely to enter into S phase. Additionally, we assessed the most significant clinical indexes of nutritional status such as body mass index and disease progression such as stage and ECOG-PS in the same cancer patient population. Cell cycle analysis of cultured unstimulated or PHA-stimulated PBMCs isolated from 120 cancer patients and 60 controls, with or without ALA, NAC, or AMI, was studied. The biological parameters relevant to cancer cachexia and OS were also studied. The addition of antioxidants ALA, NAC and AMI, enhanced significantly the progression through the cell cycle, namely from G0/G1 to S phase, of PBMCs isolated from cancer patients (+132%, +150% and +141%, respectively). The percentage of PHA-stimulated PBMCs of cancer patients entering S phase, which was significantly lower than that of controls, increased significantly to more than physiological level after coculture with antioxidants. ROS levels were significantly higher and GPx and SOD activities significantly lower in cancer patients than controls. Serum levels of IL-1 beta, IL-6, and TNFalpha were significantly higher and serum levels of IL-2 and leptin significantly lower in cancer patients than controls. Serum levels of C-reactive protein and fibrinogen were significantly higher in cancer patients than controls. A significant correlation was found in laboratory parameters only between serum levels of leptin and body mass index. Patients with advanced cancer thus exhibit both a high-grade OS and a chronic inflammatory condition. Antioxidant agents ALA, NAC, and AMI enhanced significantly the PBMCs progression through the cell cycle, thus providing evidence of their potential role in the functional restoration of the immune system in advanced cancer patients. Our data warrant further investigation with adequate clinical trials.

Adult↗
PubMed2003

IRS1 degradation and increased serine phosphorylation cannot predict the degree of metabolic insulin resistance induced by oxidative stress.

AIM/HYPOTHESIS: Oxidative stress was shown to selectively induce impaired metabolic response to insulin, raising the possible involvement of alterations in Insulin-Receptor-Substrate (IRS) proteins. This study was conducted to assess whether oxidative stress induced IRS protein degradation and enhanced serine phosphorylation, and to assess their functional importance. METHODS: 3T3-L1 adipocytes and rat hepatoma cells (FAO) were exposed to micro-molar H(2)O(2) by adding glucose oxidase to the culture medium, and IRS1 content, its serine phosphorylation and downstream metabolic insulin effects were measured. RESULTS: Cells exposed to oxidative stress exhibited decreased IRS1 (but not IRS2) content, and increased serine phosphorylation of both proteins. Total protein ubiquitination was increased in oxidized cells, but not in cells exposed to prolonged insulin treatment. Yet, lactacystin and MG132, two unrelated proteasome inhibitors, prevented IRS1 degradation induced by prolonged insulin but not by oxidative stress. The PI 3-kinase inhibitor LY294002 and the mTOR inhibitor rapamycin, but not the MEK1 inhibitor PD98059, could prevent IRS1 changes in oxidized cells. Rapamycin, which protected against IRS1 degradation and serine phosphorylation was not associated with improved response to acute insulin stimulation. Moreover, the antioxidant alpha lipoic acid, while protecting against oxidative stress-induced insulin resistance in 3T3-L1 adipocytes, could not prevent IRS1 degradation and serine phosphorylation. CONCLUSION/INTERPRETATION: Oxidative stress induces serine phosphorylation of IRS1 and increases its degradation by a proteasome-independent pathway; yet, these changes do not correlate with the induction of impaired metabolic response to insulin.

3T3 Cells↗
PubMed2004

Antioxidative treatment prevents activation of death-receptor- and mitochondrion-dependent apoptosis in the hearts of diabetic rats.

AIMS/HYPOTHESIS: The mechanisms by which glucose injures cells of the cardiovascular system include generation of reactive oxygen species and induction of cellular apoptosis. To date, little is known about the molecular events of hyperglycaemia-induced apoptosis in the heart in vivo. METHODS: Male Sprague-Dawley rats were rendered diabetic by a single intraperitoneal injection of 60 mg/kg body weight streptozotocin. Caspase activities in cardiac ventricular tissue were determined using fluorometric and immunoassay caspase-activity assay kits respectively. Expression levels of proteins of the apoptotic cascade were determined with western blot analyses using specific antibodies. RESULTS: Four weeks of hyperglycaemia induced significant apoptosis in cardiac tissue. Determining the initiators of death-receptor-dependent apoptosis revealed induction of CD95/Fas and caspase-8. Examination of the activities of effector caspases revealed increased activity of caspase-6, but not caspase-3 and -7. On evaluating inhibitors of apoptosis, we found up-regulation of caspase-3 and -7-inhibiting X-linked inhibitors of apoptosis in diabetic rats. Hyperglycaemia also induced significant mitochondrion-dependent apoptosis. Our evaluation of expression levels of Bcl-2 family members showed increased expression of pro-apoptotic Bak and Bax in diabetic rats. Antioxidative treatment with lipoic acid significantly suppressed apoptosis and down-regulated caspase-6, -8 and -9 activity, as well as expression levels of pro-apoptotic Bcl-2 proteins without changing blood glucose levels. CONCLUSIONS/INTERPRETATION: The present study indicates that reactive oxygen species induced by high glucose are involved in both death-receptor- and mitochondrion-dependent apoptosis in the heart in vivo. It also suggests that antioxidants may be a therapeutic option for preventing cardiovascular damage in diabetes mellitus in humans.

Animals↗
PubMed2002

Bacterial cysteine desulfurases: their function and mechanisms.

Cysteine desulfurase is a pyridoxal 5'-phosphate (PLP)-dependent homodimeric enzyme that catalyzes the conversion of L-cysteine to L-alanine and sulfane sulfur via the formation of a protein-bound cysteine persulfide intermediate on a conserved cysteine residue. Increased evidence for the functions of cysteine desulfurases has revealed their important roles in the biosyntheses of Fe-S clusters, thiamine, thionucleosides in tRNA, biotin, lipoic acid, molybdopterin, and NAD. The enzymes are also proposed to be involved in cellular iron homeostasis and in the biosynthesis of selenoproteins. The mechanisms for sulfur mobilization mediated by cysteine desulfurases are as yet unknown, but enzymes capable of providing a variety of biosynthetic pathways for sulfur/selenium-containing biomolecules are probably applicable to the production of cofactors and the bioconversion of useful compounds.

Bacteria↗
PubMed2006

Redox changes induced in hippocampal precursor cells by heavy ion irradiation.

Hippocampal precursors retain the capacity to proliferate and differentiate throughout life, and their progeny, immature neurons, can undergo neurogenesis, a process believed to be important in maintaining the cognitive health of an organism. A variety of stresses including irradiation have been shown to deplete neural precursor cells, an effect that inhibits neurogenesis and is associated with the onset of cognitive impairments. Our past work has shown that neural precursor cells exposed to X-rays or protons exhibit a prolonged increase in oxidative stress, a factor we hypothesize to be critical in regulating the function of these cells after irradiation and other stresses. Here we report that irradiation of hippocampal precursor cells with high-linear energy transfer (LET) 1 GeV/nucleon 56Fe ions leads to significantly higher levels of oxidative stress when compared to lower LET radiations (X-rays, protons). Irradiation with 1 Gy of 56Fe ions elicits twofold to fivefold higher levels of reactive oxygen species (ROS) compared to unirradiated controls, and at lower doses (<or=1 Gy) neural precursors exhibit a linear dose response 6 h after heavy ion exposure. The use of the antioxidant lipoic acid (LA) was able to reduce ROS levels below background levels when added before or after 56Fe ion irradiation. These results conclusively show that low doses of 56Fe ions can elicit significant levels of oxidative stress in neural precursor cells. Given the prevalence of heavy ions in space and the duration of interplanetary travel, these data suggest that astronauts are at risk for developing cognitive decrements. However, our results also indicate that antioxidants delivered before as radioprotective agents or after as mitigating agents hold promise as effective countermeasures for ameliorating certain adverse effects of heavy ion exposure to the CNS.

Animals↗
PubMed2003

Graded sensitiveness of the various retinal neuron populations on the glyoxal-mediated formation of advanced glycation end products and ways of protection.

BACKGROUND: The accumulation of advanced glycation end products (AGEs) in retinal cells is known to be associated with the risk of diabetic retinopathy. To develop a model of AGE-related metabolic stress in retinal organ cultures, we investigated the accumulation of a typical glycoxidation product (N(epsilon)-[carboxymethyl] lysine [CML]) and its possible pro-apoptotic effects on different retinal cell populations. METHODS: Retinal organ cultures (rat) were kept for 9 h in the Ames medium containing 0 (control), 5, 25, 50, 150, 300 and 800 micro M glyoxal. The expression of bax, active caspase-3, and the accumulation of CML were studied by using immunohistochemistry after the paraffin embedding of retinal explants. Apoptosis was studied using the terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick end labeling (TUNEL) test and electron microscopy. Alpha lipoic acid (alpha-LA), sodium metavanadate (NaVO(3)), N-acetylcysteine (NAC), aminoguanidine (AG), and nicotinamide (NA) were used to influence glyoxal effects in organ cultures. RESULTS: In cultured normal non-diabetic retinae, small amounts of CML and the apoptosis-promoting factors bax and active caspase-3 were present. CML, bax and active caspase-3 increased after incubation with glyoxal. Incubation with glyoxal (<300 micro M, 9 h) increased apoptotic events in all layers. At low glyoxal concentrations, we found a graded sensitiveness of the different layers: at 25 micro M 39.4% in GCL, 28.2% in INL, 11.9% in ONL. After 800 micro M glyoxal, approximately 50% of the cells in all layers of the retina were apoptotic. In the ONL, this ratio was reduced by NaVO(3) (17%), by AG (27%), by NA (24.8%), by NAC (25.2%), and by alpha-LA (33.5%). In the INL, AG (25.9%) produced the best result. In the GCL, NAC, NaVO(3) and AG reduced apoptosis. A-LA had no significant protective effect. CONCLUSION: The glyoxal-induced rapid formation of CML shows the ability of our retina model to simulate AGE-related effects in vitro. The dose-dependent expression of apoptosis-promotor molecules indicates that the apoptosis-inducing machinery starts in most retinal cells within 9 h. The neurotoxicity of glyoxal-induced AGE formation was shown by the significantly increased rate of cell death in the retina. The significant decrease of apoptotic events (P<0.01) indicates that antioxidants and AGE formation blocker can exert a differentiated cytoprotection for each of the retinal cell layers.

Acetylcysteine↗
PubMed2004

What do herbalists suggest to diabetic patients in order to improve glycemic control? Evaluation of scientific evidence and potential risks.

In the course of 12 continuing education seminars given in different regions of Italy in 2001, we distributed a questionnaire to all the attending herbalists asking information about the herbal remedy and dietary supplement they mainly recommended to subjects who required a "natural" treatment to control glycemia. We distributed 720 questionnaires and we received 685 completed ones. We have compiled a short review on the efficacy and safety of the 10 most frequently advised products for each category. The 10 more frequently suggested herbal remedies were gymnema, psyllium, fenugreek, bilberry, garlic, Chinese ginseng, dandelion, burdock, prickly pear cactus, and bitter melon. The 10 most frequently recommended dietary supplements were biotin, vanadium, chromium, vitamin B6, vitamin C, vitamin E, zinc, selenium, alpha-lipoic acid, and fructooligosaccharides. The majority of the products recommended by Italian herbalists may be efficacious in reducing glycemia. If a diabetic patient is already assuming products that even slightly reduce glycemia, we risk to underestimate the level of glucose intolerance, while if the patient stops the complementary treatment after initiating pharmaceutical therapy, in the subsequent visit we may underestimate the effect of our prescription. Therefore, if doctors are to have a role in gate-keeping or advising patients about complementary and alternative medicine, they need to be familiar with this type of medicine. If they choose otherwise, then the provision of complementary and alternative medicine will continue to be patchy and largely outside the conventional care framework, perhaps through a growing network of parallel care providers involving a large number of non-medically qualified practitioners, who patients will continue to access directly.

Blood Glucose↗
PubMed1983

Paracatalytic inactivation of pig heart pyruvate dehydrogenase complex.

The phenomenon of paracatalytic inactivation has been demonstrated and characterized with the pig heart pyruvate dehydrogenase complex. The enzyme became progressively inactive when it was preincubated in the presence of pyruvate, thiamine pyrophosphate, and extrinsic oxidative agent, 2,6-dichloroindophenol. Not only the overall reaction of enzyme complex but the individual reactions catalyzed by enzyme components, pyruvate dehydrogenase, and dihydrolipoamide acetyltrasferase, were reduced after preincubation. The observed inactivation is due to two factors: (i) covalent incorporation of the pyruvate atoms, and (ii) formation of a thiamine pyrophosphate analog. (i) A covalent incorporation of radioactivity from [2-14C]pyruvate into the enzyme complex, which was proportional to the inhibition of overall reaction was observed. Seventy-eight percent of the radioactivity incorporated into the dihydrolipoamide transacetylase but not into the lipoic acid. Thus, modification of the dihydrolipoamide acetyltransferase component can be attributed to the covalent incorporation of pyruvate atoms. (ii) During inactivation, the enzyme-bound thiamine pyrophosphate underwent a modification resulting in the formation of a thiamine pyrophosphate analog, presumably thiamine thiazolone pyrophosphate, which inhibited exclusively the pyruvate dehydrogenase component.

2,6-Dichloroindophenol↗
PubMed1988

Role of sulfhydryl groups in benzoquinone-induced Ca2+ release by rat liver mitochondria.

Incubation of rat liver mitochondria with benzoquinone derivatives in the presence of succinate plus rotenone has been shown to cause NAD(P)H oxidation followed by Ca2+ release. Further investigation revealed: (1)p-Benzoquinone-induced Ca2+ release was not initiated by a collapse of the mitochondrial membrane potential. However, Ca2+ release and subsequent Ca2+ cycling caused limited increased membrane permeability. (2) p-Benzoquinone-induced NAD(P)H oxidation and Ca2+ release were prevented by isocitrate, 3-hydroxybutyrate, and glutamate but not by pyruvate or 2-oxoglutarate. (3) Inhibition of pyruvate and 2-oxoglutarate dehydrogenases by p-benzoquinone was attributed to arylation of the SH groups of the cofactors, CoA and lipoic acid. Isocitrate dehydrogenase was also inhibited by p-benzoquinone, but the cofactors NAD(P)H and Mn2+ protected the enzyme. Glutamate dehydrogenase was not inhibited by p-benzoquinone. (4) Arylation of mitochondrial protein thiols by p-benzoquinone was associated with an inhibition of state 3 respiration, which was attributed to the inactivation of the phosphate translocase. In contrast, state 4 respiration, and the F1.F0-ATPase and ATP/ADP translocase activities were not inhibited. It was concluded that inhibition of mitochondrial NAD(P)H dehydrogenases by arylation of critical thiol groups will decrease the NAD(P)+-reducing capacity, and possibly lower the NAD(P)H/NAD(P)+ redox status in favor of Ca2+ release.

Animals↗
PubMed1996

The role of thiols in ATP-dependent transport of S-(2,4-dinitrophenyl)glutathione by rat liver plasma membrane vesicles.

The effect of thiol/disulfide exchange on ATP-dependent S-(2,4-dinitrophenyl)glutathione (GS-DNP) transport was studied in sodium nitrate treated rat liver plasma membrane vesicles. Transport followed Michaelis-Menten kinetics with an apparent Km of 9.6 microM for GS-DNP and 124 microM for ATP. 5,5'-Dithiobis(2-nitrobenzoate) (DTNB) and N-ethylmaleimide (NEM) efficiently inactivated GS-DNP transport activity in a dose- and time-dependent manner. Half-maximal inactivation occurred in 10 min at 40 microM for DTNB and 550 microM for NEM. Inactivation by DTNB was reversed by dithiothreitol. S-(N-Ethyl)maleimyl glutathione and/or ATP-Mg2+, but neither S-(N-ethyl)maleimyl cysteinylglycine nor oxidized glutathione could protect transport activity from inactivation by NEM or cystamine. These results suggest that reactive thiols are located near the active site of the transporter and that S-alkyl and the gamma-glutamyl residues of glutathione are important for protection. Biological disulfides which were tested included cystine, oxidized glutathione, oxidized Coenzyme-A, oxidized lipoic acid, and oxidized lipoamide; cystamine was the most potent reversible inactivator. Molecular oxygen also inactivated transport activity, which was recovered on addition of dithiothreitol, suggesting intramolecular disulfide formation by vicinal thiols. We interpret these results to indicate that the ATP-dependent GS-DNP transporter contains two or more thiols which are necessary for the maintenance of transport activity. The reversible inactivation of the activity by biological disulfides suggests that the transporter may be regulated by thiol/disulfide exchange in vivo.

Adenosine Triphosphate↗
PubMed1989

Single-strand cleavage of DNA by Cu(II) and thiols: a powerful chemical DNA-cleaving system.

Reduced lipoic acid, in the presence of cupric ions, introduced single-strand nicks into pSP64 plasmid DNA at micromolar concentrations, converting the supercoiled into open circular and, eventually, linear forms. The metal ion specificity of the reaction was investigated and, of Cu2+, Co2+, Cr3+, Fe3+, Fe2+, Ni2+, Mn2+ and Zn2+, only Cu2+ ions were catalysts for the thiol-induced DNA cleavage at these low concentrations. A wide range of thiols and dithiols was found to be active as DNA cleavers in the presence of Cu2+ ions.

Cations, Divalent↗
PubMed1992

Chemotaxis of human blood monocytes toward endothelin-1 and the influence of calcium channel blockers.

The adherence of monocytes to the arterial endothelium followed by its migration into the arterial intima is the earliest event in atherogenesis. The vasoconstrictive peptide, Endothelin-1 (ET-1), is elevated in patients with atherosclerosis. We were interested to know whether ET-1 was a chemoattractant for blood monocytes. Using the modified membrane filter technique for chemotaxsis assessment, ET-1 increased monocyte chemotaxis in a dose-dependent manner. Ca2+ channel blockers, Nifedipine, Diltiazem and Verapamil (5 microM), reduced ET-1 chemotaxsis more than 60% (P < 0.001). Aspirin and Indomethacin (1 mM and 100 microM, respectively) reduced migration by 23% (P < 0.05). Alpha-Lipoic acid, Probucol and Neomycin (100 microM) were also migration inhibitory (37%, P < 0.01). These results suggest that ET-1 is a strong chemoattractant for blood monocytes; Ca2+ influx is probably the major stimulus for the accelerated migration induced by ET-1.

Aspirin↗
PubMed1995

Oxidative processes and free radical scavengers in ischaemia-reperfusion injury in adipocutaneous flaps: in vitro lipid peroxidation assessment.

An in vitro lipid peroxidation study measuring Schiff base and TBAR formation in homogenates of the fat and skin fractions of epigastric free flaps of DA-rats was performed to determine the role of oxygen-derived free radicals (ODFRs) in the aetiology of ischaemic injury and of ischaemia and reperfusion injury following cold (0-1 degree C) storage. The storage intervals were 0, 48, 72, 96 and 120 h in the study on ischaemic injury and 72 and 96 h in the study on combined ischaemia and reperfusion injury. Reperfusion was accomplished by anastomosing the pedicle vessels of the flap to the femoral vessels of a recipient; the reperfusion period was 15 min. In addition to a control group (C), three experimental groups were created to test the benefit of a preischaemic single passage perfusion with a hypertonic citrate solution (HCA), a pre- and postischaemic treatment with desferrioxamine (DFX) and a pre- and postischaemic treatment with lipoic acid (LA). The susceptibility of homogenates of skin and fat fractions of epigastric free flaps in DA-rats for lipid peroxidation increased significantly whenever the cold (0-1 degree C) ischaemic interval was prolonged from 0 to 72 h. These findings offer circumstantial evidence for the role of ODFRs in the aetiology of ischaemic injury. Following a short reperfusion period after extended periods of cold (0-1 degree C) ischaemia, no significant increase in susceptibility for lipid peroxidation could be found. Furthermore, no unequivocal role in the prevention of ischaemia and/or reperfusion injury by the use of either HCA, or DFX or LA could be found. The exact role of ODFRs in the aetiology of ischaemia-reperfusion injury in this setting remains unclear.

Adipose Tissue↗