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Biomedical subjects

K Kilinç

Publications and source records attributed to K Kilinç.

At least 37 records · Page 2Linked to original sources
PubMed1999

A study of adenosine treatment in experimental acute spinal cord injury. Effect on arachidonic acid metabolites.

STUDY DESIGN: A prospective, randomized, blinded experimental trauma study. STUDY OBJECTIVE: The effect of adenosine on arachidonic acid metabolites and lipid peroxidation was investigated in induced spinal cord injury. SUMMARY OF BACKGROUND DATA: Effects of adenosine in ischemia-reperfusion models have been studied, but no studies of adenosine's effect on direct trauma to the spinal cord have been reported. METHODS: Thirty-seven adult Wistar albino rats were randomly divided into four groups and underwent laminectomy. Group 1 underwent a sham operation. Group 2 received an intravenous adenosine infusion of 100 micrograms/kg per minute for 30 minutes. In Group 3, a standard spinal cord trauma of 50 g.cm strength was established at the lower thoracic level with a "weight-drop" technique, and Group 4 received an infusion of adenosine (100 micrograms/kg per minute) for 30 minutes after the trauma. RESULTS: Tissue prostaglandin E2 activity was significantly higher in adenosine-treated trauma groups when compared with that in other groups (P < 0.0001). The difference in tissue leukotriene C4 activity between control and trauma groups was significant (P < 0.05). Adenosine infusion after trauma limited the increases in lipid peroxidation, with the difference approaching significance at P = 0.06. The structure of myelin was well preserved in the adenosine-treated trauma group. However, the changes were irreversible in severely damaged areas. CONCLUSION: After acute spinal cord trauma, intravenous adenosine infusion of 100 micrograms/kg per minute could attenuate progression to secondary injury, but adenosine alone was not effective yet.

Acute Disease↗
PubMed1999

Angiotensin converting enzyme gene polymorphism and activity in Turkish patients with essential hypertension.

Studies in various ethnic groups have shown contradictory evidence on the association of the angiotensin converting enzyme (ACE) insertion/ deletion (I/D) polymorphism with essential hypertension. We conducted a case-control study in Samsun, Turkey, to examine the association between ACE genotype, ACE serum activity, and blood pressure. Serum ACE activity was measured and ACE I/D polymorphism performed in 165 hypertensive and 143 normotensive subjects. Genomic DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). PCR primers were flanking the polymorphic region in intron 16 of the ACE gene. The distribution of the DD, ID, and II ACE genotypes was 65, 77, and 23 in hypertensive patients and 42, 82, and 19 in normotensive subjects (P > .05). The estimated frequency of the insertion allele was 0.37 in hypertensive and 0.42 in normotensive subjects. Nevertheless, sensitivity analysis, based on positive family history and severity of hypertension, suggested that significant associations existed between more homogeneous groups of hypertensives and normotensives (P < .05). ACE genotype influenced ACE activity and the highest level was in DD genotype, being the lowest in II genotype. ACE serum levels were significantly higher in hypertensives as compared with normotensives (P < .01). A modest correlation was observed between blood pressure and ACE among hypertensive persons (r = 0.25, P < .05) and this did persist in multivariate analysis (P < .05 for systolic blood pressure and P < .005 for diastolic blood pressure). These data suggest that ACE DD genotype may have predisposing effects on severe hypertensives and cases with positive family history, and that ACE may be one of the independent factors on hypertension.

Adult↗
PubMed1999

Antioxidant action of the antiarrhythmic drug mexiletine in brain membranes.

Mexiletine is a class Ib antiarrhythmic drug used in the treatment of ventricular arrhythmias. The Na+ channel blocker mexiletine inhibits calcium influx in cells via decreasing reverse operation of the Na+-Ca2+ exchanger. Thus this drug is shown to protect the CNS white matter against anoxic/ischemic injury. The aim of our study was to investigate if this drug could act as an antioxidant drug as well. The antioxidant action of this drug was studied under different oxidant conditions in vitro, and thiobarbituric acid-reactive substances were measured to follow lipid peroxidation. Mexiletine inhibited iron-ascorbate-H2O2-induced lipid peroxidation in brain membranes, liver microsomes and phospholipid liposomes, being most effective in brain membranes. The inhibition was dose- and time-dependent. Mexiletine also inhibited copper-ascorbate-H2O2-induced lipid peroxidation but to a lesser extent. It is concluded that mexiletine has a dual effect toward oxidative injury in brain, both by inhibiting Na+-Ca2+ exchanger-dependent Ca2+ influx and by acting as an inhibitor of lipid peroxidation. However, as this drug is effective at millimolar concentrations, it should be considered less active than natural antioxidants that are effective at micromolar concentrations.

Animals↗
PubMed1998

Antioxidant therapy of cobalt and vitamin E in hemosiderosis.

The protective effects of cobalt and vitamin E in iron overloaded rats were investigated. Rats were divided into four groups: group 1 as control, group 2 received only iron; group 3 iron and cobalt, group 4 iron and vitamin E. All injections were given 3 times per week for 3 weeks. Biochemical and histopathologic studies were done on samples of blood and liver, spleen, and intestine. The results showed that the administration of iron with cobalt or vitamin E decreased lipid peroxidation and the levels of hypoxanthine in all tissues (P < .001). Tissue associated myeloperoxidase (MPO) activity was increased in all iron-overloaded animals. However, vitamin E and cobalt decreased MPO activity (P < .001) in all tissues with the exception of the intestines, where cobalt was ineffective. Cobalt therapy increased hemoglobin, hematocrit, and MCV (P < .05). In contrast to SGPT activity, SGOT activity was significantly increased in all groups but more so in group 3 animals. The increased activity of serum SGOT levels might be related to the mechanical injury by cardiac puncture. The most striking histopathologic finding was the presence of granulomas in the livers of 71% of the animals of group 2 and in 66.6% of group 3. Interestingly, granulomas developed in only 33.3% of group 4 animals, whereas no granulomas were found in the livers of control animals (group 1). In this article we report that cobalt is as effective as vitamin E in significantly reducing iron-induced biochemical changes in an iron-overload in vivo model. We further describe for the first time the presence of extensive granuloma formation in iron-overloaded liver tissue and the greater efficiency of vitamin E over cobalt in protecting against granuloma formation in iron overload.

Alanine Transaminase↗
PubMed1998

Experimental study of the effect of adrenaline tolerance on intestinal ischaemia-reperfusion.

BACKGROUND: Adrenaline tolerance improves survival in animal models of shock. The purpose of this study was to determine the effects of adrenaline tolerance on intestinal ischaemia-reperfusion in a mouse model. METHODS: Adrenaline tolerance was developed by injecting intravenous adrenaline, gradually increasing the dose to 2 mg/kg over 5 days. In experimental animals the superior mesenteric artery was clamped for 120 min and then released. Evans blue dye was given intravenously to all animals to quantify pulmonary microvascular injury. Some 60 min after clamp release, the animals were killed and the effects of reperfusion assessed on tissue samples. RESULTS: Evans blue dye concentrations were significantly higher in animals with intestinal ischaemia-reperfusion than in those having sham intestinal ischaemia-reperfusion or in adrenaline-tolerant mice having intestinal ischaemia-reperfusion or sham ischaemia-reperfusion (P< 0.01). Malonyldialdehyde levels increased significantly in the lung in the intestinal ischaemia-reperfusion group compared with those in the sham ischaemia-reperfusion group (P< 0.001 for liver, lung and small intestine), whereas there was no difference in adrenaline-tolerant animals. There was no significant change induced by adrenaline tolerance in myeloperoxidase levels in any organ. CONCLUSION: Adrenaline tolerance reduced the lung permeability caused by intestinal ischaemia-reperfusion. Catecholamines may play a role in free radical generation induced by ischaemia-reperfusion.

3,4-Methylenedioxyamphetamine↗
PubMed1998

Beneficial effect of captopril against ischaemia-reperfusion injury in isolated guinea pig hearts.

The study was designed to clarify whether captopril, an angiotensin-coverting enzyme inhibitor, will reduce the injury of global ischaemia and reperfusion after cardioplegic arrest in isolated guinea pig hearts, in a modified Langendorff model. The hearts were randomly allocated into four groups (n = 10 in each) and subjected to 90 min of normothermic global ischemia, followed by 30 min of reperfusion; in all groups, cardioplegic arrest was achieved by administering St. Thomas's Hospital cardioplegic solution (STHCS). The first group was utilized as the control group. In the second group, captopril (200 mumol/L) was added to STHCS. In the third group, oral pretreatment was carried out (0.3 mg/kg captopril was given twice a day for 10 days). In the fourth group, oral pretreatment was achieved and captopril-enriched solution was applied in the first 5 min of reperfusion. Although the study groups showed better recovery of contractility than the control group, in the fourth group the hearts had the best left ventricular contractile function, where contractile force (g contractility/g heart weight) was 55.4% +/- 3.8% of the preischameic values. Groups I, II, and III achieved 31.0% +/- 3.2%, 41.6% +/- 3.8%, and 48.3% +/- 3.9% of their preischaemic contractile force values. Creatine kinase leakage was significantly lower and postischaemic coronary flows, too, were significantly higher in the fourth group. Coronary flow after reperfusion increased from 48.5 +/- 6.7 to 65.2 +/- 7.1 ml/min g heart in group 4 (p < 0.05). Myocardial lipid peroxides and glutathione contents showed that there was a correlation between the depletion of myocardial glutathione content and increased lipid peroxidation. These preliminary results showed that: the addition of captopril to reperfusion solution and oral preconditioning improved post-ischameic myocardial function and decreased myocardial injury.

Administration, Oral↗
PubMed1998

Time-level relationship for lipid peroxidation and the protective effect of alpha-tocopherol in experimental mild and severe brain injury.

OBJECTIVE: Oxygen free radical-mediated lipid peroxidation has been proposed to be one of the major mechanisms of secondary damage in traumatic brain injury. The first purpose of this study was to establish the time-level relationship for lipid peroxidation in injured brain tissue. The second purpose was to examine the protective effect of alpha-tocopherol against lipid peroxidation. METHODS: For this study, 65 guinea pigs in five groups were studied. Five of the animals were identified as a control group, and the remaining 60 animals were divided equally into four groups (Groups A, B, C, and D). Mild injury (200 g x cm) (Groups A and C) and severe injury (1000 g x cm) (Groups B and D) were produced by the method of Feeney et al. Alpha-tocopherol (100 mg/kg) was administered intraperitoneally before brain injury in Groups C and D. Five animals from each group were killed immediately after trauma, five after 1 hour, and the remaining five animals after 36 hours. Lipid peroxidation in traumatized brain tissues was assessed using the thiobarbituric acid method. RESULTS: In all groups with traumatic brain injuries, levels of malondialdehyde, a lipid peroxidation product, were higher than in the control group. The amount of lipid peroxidation was increased by the severity of the trauma. Alpha-tocopherol significantly suppressed the rise in lipid peroxide levels in traumatized brain tissues. CONCLUSION: This study demonstrates that lipid peroxidation is increased by the severity of trauma and that alpha-tocopherol has a protective effect against oxygen free radical-mediated lipid peroxidation in mild and severe brain injury.

Animals↗
PubMed1998

Molecular size distribution analysis of human gingival proteoglycans and glycosaminoglycans in specific periodontal diseases.

In order to determine the molecular-size distribution of gingival proteoglycans (PGs) and glycosaminoglycans (GAGs) both in periodontal health and disease states, gingival tissues were obtained from patients with early onset periodontitis (EOP) and adult periodontitis (AP) and also from periodontally healthy subjects. Gel filtration chromatography of gingival PGs revealed different profiles for periodontally diseased and healthy gingiva. Healthy gingiva was mainly composed of high-molecular size proteins and PGs, while diseased gingival tissue presented a decrease in high-molecular size PG forms and a shift towards low-molecular size proteins and PGs. This indicates the degradation of PG macromolecules during periodontal disease activity. Furthermore, this shift towards low-molecular size forms was more intense in EOP patients when compared to AP patients. Gel filtration of gingival GAGs also demonstrated depolymerization of GAGs, with low-molecular size GAGs being more intense in periodontally diseased gingiva, while healthy gingival GAGs profile was mainly composed of high-molecular size GAGs. Similar to the profile of gingival PGs, low-molecular size gingival GAGs were more prominent in gingival tissue from patients with EOP. These findings suggest that both PGs and GAGs, essential components of the extracellular matrix (ECM), are depolymerized during periodontal disease activity, which is more prominent in EOP. Since the basic feature of periodontal disease is matrix degradation, ECM components, more specifically PGs and GAGs, are likely to provide valuable information for a better understanding of periodontal disease activity.

Adult↗
PubMed1998

Effect of carnitine supplementation on cardiac function in hemodialyzed children.

Thirteen carnitine-deficient children (mean age, 16.1 +/- 2.56 years) on a three-times-weekly hemodialysis program for at least 1 year, and 11 healthy age matched children were involved in the study. All the patients had stable blood pressure and hemoglobin (Hb) levels with a maintenance dose of erythropoetin and none were digitalized. The total carnitine (TC) and free carnitine (FC) plasma levels were sampled prior to hemodialysis (HD) before and after 3 months of carnitine supplementation. A free carnitine (FC) to acylcarnitine (AC) ratio less than 4 was defined as carnitine deficiency. Intravenous L-carnitine was injected at a dose of 20-40 mg/kg three times weekly at the end of each dialysis session for a 3-month period. Echocardiographic examination was performed the day following HD, before and after carnitine treatment. Systolic and diastolic functions of the left ventricle, including the ejection fraction, were measured. Almost all the parameters were significantly different in controls and hemodialyzed patients. In carnitine-deficient hemodialyzed patients, 3 months of L-carnitine supplementation resulted in a significant increase in blood carnitine levels and the FC/AC ratio, but this was not associated with any significant improvement of cardiac function. Furthermore no significant changes were observed in plasma triglycerides, total cholesterol or other lipoprotein parameters before or after carnitine supplementation. Although there was a moderate increase in mean hematocrit (Hct) and Hb levels, these also did not reach statistically significant levels. These results suggest that the 3 months of carnitine supplementation is not sufficient to ameliorate cardiac function or increase Hb levels in children.

Adolescent↗
PubMed1997

Histidine modification of human serum butyrylcholinesterase.

The effects of histidine-modifying reagents on human serum butyrylcholinesterase (BChE) were investigated. The commercially available enzyme was further purified by chromatography on a Sepharose CI-6B column prior to use. In the modification studies, we found that the histidine-specific reagents tosylphenylalanine chloromethyl ketone (TPCK) and tosyllysine chloromethyl ketone (TLCE) did not modify the enzyme; however, they inhibited the enzyme reversibly. The kinetic parameters of enzyme inhibition calculated were alpha = 10.8, beta = 0.26, and Ki = 0.016 mM for TPCK. TLCK inhibition gave similar kinetic behavior, with alpha = 41.6, beta = 0.065, and Ki = 0.039 mM. Tosyllysine, an analog of TLCK, did not inhibit the enzyme. Removal of TPCK and TLCK by dialysis resulted in significant reactivation of the enzyme. From kinetic studies, it was found that the inhibitions were hyperbolic mixed-type inhibitions. We concluded that the reagents competed with substrate for hydrophobic binding sites and inhibited the enzyme reversibly. On the other hand, in the modification studies with diethyl pyrocarbonate (DPC), it was observed that inactivation of the enzyme was irreversible and time-dependent. In the protection studies, the activity of the enzyme was partially protected from inactivation by DPC even at a 50 mM concentration of butyrylthiocholine. The results indicate that DPC modifies some essential histidine side chains in BChE, including the functional histidyl residue found at the active site.

Binding Sites↗
PubMed1997

Torsion of only spermatic cord in the absence of testis and/or epididymis results in contralateral testicular hypoxia.

Unilateral spermatic cord torsion in the presence or absence of ipsilateral testis causes hypoxia in the contralateral testis. An experimental study was conducted to find the most important structure that causes contralateral testicular hypoxia following ipsilateral twisting. In five groups each consisting of 10 rats sham operations, epididymoorchiectomy, spermatic cord torsion, spermatic cord torsion following subepididymal orchiectomy or spermatic cord torsion following epididymoorchiectomy were performed. Lactic acid, hypoxanthine and thiobarbituric acid reactive products of lipid peroxidation (TBAR) were determined in the contralateral testis. While lactic acid, hypoxanthine and TBAR values did not differ significantly following sham and epididymoorchiectomy procedures, evaluation of other groups revealed significantly increased values compared with sham and epididymoorchiectomy groups. Since torsion of only spermatic cord and testicular vasculature causes contralateral testicular hypoxia, testis and epididymis do not seem to be mandatory for occurrence of contralateral testicular hypoxia. Testicular artery under distress seems to be the most important structure that results in contralateral testicular hypoxia following torsion.

Animals↗
PubMed1997

Propofol attenuates formation of lipid peroxides in tourniquet-induced ischaemia-reperfusion injury.

We studied 20 adult ASA I patients undergoing elective peripheral surgery allocated randomly to one of two groups. In the propofol group (n = 9) anaesthesia was induced with propofol and fentanyl followed by continuous infusion of propofol. In the control group (n = 11), after induction of anaesthesia with thiopentone and fentanyl, anaesthesia was maintained with isoflurane. Concentrations of lipid peroxides in both plasma and muscle tissue samples were measured as thiobarbituric acid-reacting substances (TBARS). Plasma TBARS concentrations increased significantly in the control group at 1, 5, 15, 30 and 45 min after release of the tourniquet to mean 1.83 (SD 0.13), 2.00 (0.12), 2.25 (0.14), 2.30 (0.12) and 2.41 (0.14) mumol litre-1, respectively, compared with pre-reperfusion values (1.64 (0.14) mumol litre-1). In the propofol group this was significant only at 30 min (1.85 (0.03) vs 1.74 (0.04) mumol litre-1). TBARS concentrations of reperfused muscle tissue were significantly higher than pre-reperfusion concentrations in the control group (70.30(10.06) vs 52.13 (5.73) nmol/g wet tissue). We conclude that propofol attenuated ischaemia-reperfusion-induced lipid peroxidation in the therapeutic doses used in anaesthesia.

Adult↗
PubMed1997

A new model for tethered cord syndrome: a biochemical, electrophysiological, and electron microscopic study.

In order to investigate the pathophysiology of the tethered cord syndrome, a few experimental models have been developed and used previously. In this study, the authors present a new experimental model to investigate the biochemical, electrophysiological, and histopathological changes in the tethered spinal cord syndrome. A model was produced in guinea pigs using an application of cyanoacrylate to fixate the filum terminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were performed on 40 animals divided into two groups. The responses to tethering were evaluated with hypoxanthine and lipid peroxidation, somatosensory and motor evoked potentials, and transmission electron microscope examination. The hypoxanthine and lipid peroxidation levels significantly increased, indicating an ischemic injury (p < 0.01). The average hypoxanthine level in the control group was 478.8 +/- 68.8 nmol/g wet tissue, while it was 651.2 +/- 71.5 nmol/g in the tethered cord group. The lipid peroxidation level in group I was 64.0 +/- 5.7 nmol/g wet tissue, whereas it was 84.0 +/- 4.7 nmol/g in group II. In the tethered cord group, the latencies of the somatosensory and motor evoked potentials significantly increased, and the amplitudes decreased. These changes indicated a defective conduction in the motor and sensorial nerve fibers. In the transmission electron microscopic examinations, besides the reversible changes like edema and destruction in the gray-white matter junction, irreversible changes like scarcity of neurofilaments and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for tethered cord syndrome.

Animals↗
PubMed1996

Effect of Nd:YAG laser on experimental disc degeneration. Part I. Biochemical and radiographical analysis.

Intervertebral disc herniation is an important health problem from both the social and economic aspect. It is often accompanied by a decrease in the content of water and proteoglycan (PG). The present study was undertaken to elucidate the effect of neodymium-yttrium-aluminum-garnet (Nd:YAG) laser on degenerated disc tissue. In this study a ventral disc herniation model in guinea pigs was performed to study the effects of ND:YAG laser on degenerated disc with low water and PG content. Effect of ND:YAG laser on degenerated cervical disc tissue is examined from the aspects of biochemistry and radiology. In the acute period water, PG, and collagen content decreased due to the ablative effect of ND:YAG laser on disc tissue. When changes in the degenerated disc in the post-laser chronic period were compared with degenerated disc findings, statistically significant changes could not be be found. From the results of this study, there is no question that the Nd:YAG laser offers many potential benefits, it remains to be proven whether or not this is of real benefit in the treatment of patients with degenerated disc disease.

Analysis of Variance↗
PubMed1996

Tissue hypoxia in ipsilateral and contralateral testes undergoing surgically induced maldescent.

The mechanism of deterioration of ipsilateral and contralateral testes during unilateral maldescent remains controversial. Proposing that alterations in tissue perfusion may play a role in ipsilateral and contralateral testicular deteriorations, an experimental study has been planned to evaluate the status of parameters of tissue hypoxia in ipsilateral and contralateral testes following surgically induced maldescent, in rats which preoperatively underwent placebo or chemical sympathectomy. 60 male albino rats were used for the experiment. At the age of 21 days each 30 rats that were treated by placebo or chemical sympathectomy agent were divided into 3 groups undergoing sham operation, abdominal fixation of one testis or abdominal fixation of both testes. At the age of 3 months the rats underwent bilateral orchidectomies and lactic acid (LA) and hypoxanthine (HX) levels were measured in testicular tissues. Maldescent of the testis resulted in a marked increase of LA and HX values in the ipsilateral testis compared to controls, and also resulted in increased levels of LA and HX in the contralateral testis. Although the levels of LA and HX were lower compared to ipsilateral undescended counterparts the levels in contralateral testis were significantly elevated compared to the contralateral testes of rats undergoing sham operation following placebo treatment. Bilateral maldescent resulted in similar elevations of LA and HX in both of the testes. Administration of 6-hydroxydopamine did not result in decreased levels of LA and HX values in the ipsilateral testis following unilateral testicular undescendence. However the LA levels in the contralateral descended testis did not reveal a significant difference compared to the contralateral testis of rats undergoing sham operation. The present experimental design reveals that abdominal fixation of the testis results in tissue hypoxia not only in the ipsilateral but also in the contralateral testis. Chemical sympathectomy has some protective effects on contralateral testicular hypoxia during unilateral maldescent. Tissue hypoxia during maldescent may result from relative inadequacy of testicular blood flow to overcome the increased metabolic demands under hyperthermic conditions.

Animals↗
PubMed1995

Is ipsilateral testis mandatory for the occurrence of contralateral intratesticular biochemical changes indicative of hypoxia after unilateral spermatic cord torsion?

Experimental unilateral spermatic cord torsion has been shown to induce both ipsilateral and contralateral intratesticular biochemical changes indicative of hypoxia. An experimental study was conducted to see whether the presence of the ipsilateral testicular tissue is necessary for the occurrence of the biochemical changes in the contralateral testis. Male, adult, albino rats were divided into four groups each containing 10 rats. One group served to determine basal values of biochemical parameters indicative of tissue hypoxia, another group was subjected to unilateral spermatic cord torsion in the presence of ipsilateral testis; a further group was subjected to unilateral spermatic cord torsion after ipsilateral subepididymal orchiectomy, and the last group underwent unilateral subepididymal orchiectomy alone as control. Lactic acid, hypoxanthine and lipid peroxidation product levels which are biochemical indicators of tissue hypoxia were determined in testicular tissues and kidneys. All three parameters increased significantly in contralateral testes but not in kidneys after unilateral spermatic cord torsion both when the ipsilateral testis was present and absent (p < 0.05). It is concluded that the ipsilateral testis does not play a role in transmitting these contralateral changes after unilateral spermatic cord torsion. Impulse-triggering contralateral changes may arise from spermatic vessels or nerves.

Animals↗
PubMed1995

The effect of high dose antenatal vitamin E on hypoxia-induced changes in newborn rats.

The protective effects of high dose antenatal vitamin E on hypoxemia in newborn rats were investigated. The subjects were 1-d-old Wistar rats weighing 5-6 g which were born to mothers weighing 245-250 g. Three groups of rat pups, each consisting of eight newborn rats, were used: nontreated control group, hypoxic group, and vitamin E group. The mothers of pups in the last group were given vitamin E (2000 mg/kg/d) antenatally on 3 consecutive days. Hypoxia was induced by breathing of a mixture of 8% oxygen and 92% nitrogen for 3 h. Then pups were allowed to inhale normal atmospheric air for 30 min. All rats were killed on the first day of life after the procedure of hypoxia and reoxygenation. The brains, lungs, livers, intestines, and kidneys were studied biochemically and histopathologically. The hypoxia-induced biochemical changes were determined by measuring lipid peroxidation and myeloperoxidase activity. Vitamin E effectively inhibited hypoxia-induced lipid peroxidation in liver and intestines, and decreased the levels of thiobarbituric acid-reactive substances in brain. In agreement with lipid peroxidation, tissue associated myeloperoxidase activity was increased in liver, intestines, and kidneys, but not in brain and lungs, of the hypoxic group. Histopathologic changes in intestines were epithelial separation and submucosal polymorphonuclear leukocyte infiltration. In the liver, leukocyte infiltration was observed only near the portal areas. These changes were not observed in the vitamin E group. It was concluded that high doses of antenatal vitamin E may protect the newborn rat pups against hypoxia-induced tissue injury.

Animals↗