The effects of resveratrol on hepatic oxidative stress in metabolic syndrome model induced by high fructose diet.

BACKGROUND: The purpose of this study was to evaluate probable protective effects of resveratrol treatment on hepatic oxidative events in a rat model of metabolic syndrome (MetS). METHODS: Thirty-two male adult rats were randomly divided into 4 groups: control, fructose, resveratrol, and fructose plus resveratrol. To induce MetS, fructose solution (20 % in drinking water) was used. Resveratrol (10 mg/kg/day) was given by oral gavage. All treatments were given for 8 weeks. Serum lipid profile, glucose and insulin levels, liver total oxidant status (TOS) levels and paraoxonase (PON), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) activities were analyzed. RESULTS: Fructose-fed rats displayed statistically significant increases in TOS levels, and decreases in PON activity compared to the control group. Resveratrol treatment moderately prevented the decrease in liver PON activity caused by fructose. On the other hand, resveratrol, alone or in combination with fructose, did not change the TOS levels when compared to the fructose group. The SOD and CAT activities in all groups did not change. CONCLUSION: In this experimental design, high-fructose consumption led to elevated TOS levels and low PON activities. The resveratrol therapy shown beneficial effects on PON activity. However, it was found to behave like a prooxidant when administered together with fructose and alone in some parameters. Our results can inspire the development of new clinical therapy in patients with MetS (Tab. 2, Ref. 34).

The investigation of melatonin effect on liver antioxidant and oxidant levels in fructose-mediated metabolic syndrome model.

OBJECTIVE: Metabolic syndrome (MetS) can be induced by the oxidative stress conditions caused by ingestion of large amounts of fructose. We investigated the possible protective effects of melatonin administration on liver tissues in fructose-fed rats. MATERIALS AND METHODS: Thirty-two rats were randomly divided into four groups; control, fructose, melatonin, and fructose plus melatonin. MetS was induced by a fructose solution (20% in tap water) and melatonin (20 mg/kg daily) was administered by oral gavage. Systolic blood pressures (SBP) were measured. After the end of the 8-week experimental period, serum lipid profile, glucose and insulin levels, tissue total oxidant status (TOS) and activities of paraoxonase (PON), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were measured. RESULTS: Fructose consumption significantly increased SBP, serum triglyceride and insulin levels and induced insulin resistance, confirming successful establishment of the MetS model. After fructose administration, the TOS levels and GSH-Px activities significantly increased in all groups compared to the control group. The PON activity in the fructose group significantly decreased compared to the control group. Melatonin supplementation, with or without fructose, increased PON activity. The SOD activity significantly increased in the fructose group compared to the control group, but significantly decreased in the melatonin group compared to the control and fructose groups. CAT activity was unchanged in all groups. CONCLUSIONS: GSH-PX and PON are important antioxidants for reducing oxidant stress. Melatonin might act as a prooxidant at the dose given in our experimental design when administered with fructose.

The effect of experimental diabetes on the circadian pattern of adenosine deaminase and myeloperoxidase activities in rat liver.

This study investigated time-dependent variations in the activities of adenosine deaminase (ADA), an adenosine-metabolizing enzyme, and myeloperoxidase (MPO), an oxidation reaction-catalyzing enzyme, in control and streptozotocin (STZ)-induced diabetic rat liver. The animals were sacrificed at six different times of day (1, 5, 9, 13, 17 and 21 hours after lights on - HALO). The hepatic activity of ADA did not change depending on the STZ treatment whereas MPO activity was significantly higher in the diabetics than in the controls. Hepatic ADA activity was dependent on the time of sacrifice with the lowest activity at 21 HALO and the highest activity at 5 HALO. Both enzyme activities failed to show any significant interaction between STZ treatment and time of sacrifice, which means that diabetes does not influence the 24 h pattern of these activities. Since MPO, a heme protein localized in the leukocytes, is involved in the killing of microorganisms, increased MPO activity in diabetic rat liver may reflect leukocyte infiltration secondary to diabetes. A reduction in ADA activity during the dark (activity/feeding) period will presumably lead to high concentrations of adenosine in the liver, possibly contributing to changes in some metabolic processes, such as glycogen turnover and oxygen supply.

The effect of taurine on polymorphonuclear leukocyte functions in endotoxemia.

The aim of the present study was to measure MPO activity in PMN leukocytes after endotoxin administration, and to compare the levels of NO2- competing with taurine for reaction with HOCl. Furthermore we aimed to determine TauCl levels, a product of MPO-H2O2-Halide system, and to evaluate anti-inflammatory properties of PMN in endotoxemia. In addition, our second objective was to investigate the effect of taurine, an antioxidant amino acid, on anti-bactericidal and anti-inflammatory functions of PMN after administration of endotoxin together with taurine. All experiments were performed with four groups (control, taurine, endotoxemia, and taurine plus endotoxin) of ten guinea pigs. After endotoxin administration (4 mg/kg), MPO activities increased and taurine levels decreased. Therefore levels of TauCl, NO2*- increased. We observed the effects of taurine as conflicting. When taurine was administrated alone (300 mg/kg), all of these parameters decreased.Consequently, we suggested that taurine is influential in infected subjects but not on healthy ones as an antioxidative amino acid. In addition, we believe that in vivo effects of taurine may differ from those in vitro depending on its dosage.

Protective effect of taurine on respiratory burst activity of polymorphonuclear leukocytes in endotoxemia.

The aim of this study was to evaluate the effect of endotoxin on PMN leukocyte respiratory burst activity by measuring G6PD, NADPH oxidase and XO activities in guinea pig. In addition, the possible protective role of taurine against endotoxin-mediated PMN leukocyte function was examined. All experiments were performed with four groups (control, taurine, endotoxemia, taurine plus endotoxin) of ten guinea pigs. After the endotoxin was administrated (4 mg/kg) both G6PD and NADPH oxidase activities were significantly reduced compared with the control group. NADPH oxidase activity returned to the control value and G6PD activity also increased but it did not reach the control value. However when taurine was administrated (300 mg/kg) the activity of NADPH oxidase reached the control value; furthermore, G6PD activity also increased but it could not reach to the control value. When taurine was administrated alone, no effect on these enzymes was observed. Following the endotoxin administration, the activity of XO considerably increased. When taurine was administrated together with endotoxine and alone, this activity decreased compared to control value in both conditions. These results indicate that the O2*- formation in PMN leukocytes after the endotoxin administration is ensured by the catalysis of XO due to the inhibited NADPH oxidase activity. It was observed that taurine has considerable anti-inflammatory and antioxidant effects. However, conflicting results were obtained when taurine was administrated alone or together with an oxidant agent.

Role of free radicals on mechanism of radiation nephropathy.

PURPOSE: In our study, after applying a single dose of 612 cGy irradiation, we aimed to observe the role of free radicals on tissue damage in the kidney caused by radiation by measuring NO level, Na/K-ATPase activity and TBARS amount which is an indicator of free radical damage. On the other hand we investigated whether the tissue damage can be prevented by vitamin A or not. MATERIALS AND METHODS: This study was performed on three groups: 1. Control group 2. The group to which irradiation was administrated 3. The group which was given radiation + vitamin A. The irradiation group of animals were given a single dose of gamma irradiation at a sublethal dose. In the group which was administrated both irradiation + vitamin A, vitamin A was given for two days prior to irradiation. The amount of NO was measured by ESR spectroscopy, Na/K-ATPase and TBARS were measured by spectrophotometry. RESULTS AND CONCLUSIONS: As a result of radiation mediated tissue damage in the kidney, we observed a NO loss, a decrease in Na/K-ATPase activity and an increase in TBARS amount. Although the administration of vitamin A before radiation, did not have any effect on NO loss and decrease in Na/K-ATPase.

Delayed energy protection of ischemic preconditioning on hepatic ischemia/reperfusion injury in rats.

BACKGROUND: Hepatic ischemia/reperfusion (IR) injuries associated with hepatic resections are unresolved problems in the clinical practice. The aim of this study is to elucidate the effect of ischemic preconditioning (IPC) on the energy charge (EC) and related mechanisms at the late phase of hepatic IR injury. METHODS: 30 Wistar rats were randomly divided into sham, IR and IPC groups. The model of partial hepatic IR was used. The rats were subjected to 60 min hepatic ischemia, pretreated by IPC (10/15 min) or not. After 24 h of reperfusion, serum alanine aminotransferase (ALT), nitrite/nitrate (NOx), malondialdehyde (MDA), hepatic tissue arginase activity, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and EC of the liver were measured. RESULTS: Liver injury reduced by IPC is measured by liver tissue arginase activity and serum ALT. Tissue NOx levels in rats pretreated with IPC were significantly higher than levels in the IR group (p < 0.001). Tissue levels of MDA in the liver of the IPC group were found to be significantly lower than the levels in the IR group (p < 0.001). ATP and EC levels 24 h after hepatic ischemia in rats pretreated with IPC were higher than the levels in the IR (p < 0.05). All groups had similar ADP and AMP levels in the liver tissues. The IPC procedure significantly reduced the hepatic necrosis (p < 0.001). CONCLUSION: The results of this study demonstrated that pretreatment with IPC improved tissue ATP, EC, and hepatic necrosis at late stages of ischemia reperfusion injury of the liver. Increased nitric oxide, reduced MDA and arginase activity seemed to play a regulatory role in this delayed protective effect of IPC.

The effect of Escherichia coli-derived lipopolysaccharides on plasma levels of malondialdehyde and 3-nitrotyrosine.

The aim of this study was to determine the effect of Escherichia coli (E. coli)-derived lipopolysaccharide on rat plasma low density lipoprotein (LDL), malondialdehyde and 3-nitrotyrosine levels (an indicator of protein nitration). Six hours after intraperitoneal administration of E.coli, plasma LDL was measured electrophoretically and malondialdehyde level was measured by spectrophotometric method. Plasma malondialdehyde was significantly (p<0.001) elevated in E. coli-injected rats (4.97 +/- 1.33; n=10) in comparison to control animals (1.83 +/- 0.5; n=10). In addition, plasma 3-nitrotyrosine level, determined by reverse-phase HPLC, was also increased in the infected group (2.84 +/- 1.17 to 0.22 +/- 0.13; n=10). This increase was statistically significant (p<0.001). An increased level of oxidation of lipids and 3-nitrotyrosine was observed as a result of free radical-mediated damage in plasma. In conclusion, asymptomatic infections may increase the risk of atherosclerosis by inducing free radical formation and a consequent increase in the oxidation of LDL.

Changes in zinc levels and superoxide dismutase activities in the skin of acute, ultraviolet-B-irradiated mice after treatment with ginkgo biloba extract.

Acute ultraviolet-B (UV-B) irradiation is known to act as an initiator in the formation of reactive oxygen species. These oxygen products are highly reactive and they are able to cause irreversible damage to cellular components. Oxygen free radicals are normally neutralized by very efficient systems in the body. These include antioxidant enzymes like superoxide dismutase (SOD). In a healthy subject, there is a balance between free radicals and the levels of antioxidants. In some pathological conditions such as oxidative stress, the level of antioxidants is significantly reduced. The skin contains relatively high levels of zinc (Zn), an essential element known to be a cofactor in some metabolic pathways. Zinc has also been reported to have antioxidant properties. In the present study, we investigated the effect of ginkgo biloba extract (Gbe), a potent free-radical scavenger, on UV-B-irradiated skin by measuring SOD activity and Zn levels in the skin, before and after treatment. The SOD activity was decreased after UV-B exposure, in comparison with the control group (p < 0.05). After Gbe treatment, the SOD activity increased (p < 0.05) as compared with the untreated UV-B irradiated group. The Zn levels changed in the same pattern as the SOD activity values.

The effects of peroxynitrite on erythrocytes.

Endotoxin-induced peroxynitrite formation has been demonstrated in plasma. The aim of this study is to evaluate whether this has an effect on erythrocytes. For this purpose erythrocyte 3-nitrotyrosine (3-NT) level, Na+-K+ ATPase and glutathione peroxidase activities were measured both in vivo and in vitro. In vivo peroxynitrite formation was induced in rats by intraperitoneal Escherichia coli (E.coli) injection. Erythrocytes were directly incubated with peroxynitrite in the in vitro experiment. 3-NT levels were measured by reverse-phase HPLC, glutathione peroxidase, and Na+-K+ ATPase activities were measured by spectrophotometric techniques. There was a marked increase in the 3-NT levels in both experiments. However, glutathione peroxidase activity was significantly increased in in vivo experiments, while decreasing in in vitro conditions. Although Na+-K+ ATPase activities were significantly reduced by peroxynitrite in vitro, Na+-K+ ATPase activities were similar in control and E.coli-injected rat erythrocytes. Although nitrating effect of peroxynitrite does not seem to be preventable by endogenous antioxidants, this effect of peroxynitrite may not endanger erythrocytes if the oxidative damage of peroxynitrite is prevented.

An alternative parameter for monitoring the therapeutic benefits of allopurinol simultaneously in renal ischaemia-reperfusion injury: MDA/ATP Ratio.

The therapeutic benefits of allopurinol pretreatment in renal ischaemia-reperfusion injury were investigated by monitoring renal malondialdehyde (MDA) and ATP levels together with calculated MDA/ATP ratio in ischaemic (45 min) and reperfused (15 min) rat kidneys. MDA levels remained unchanged during ischaemia, but increased after the subsequent reperfusion. ATP content of the ischaemic kidney was decreased significantly and the recovery of ATP was incomplete after the reperfusion, whereas the MDA/ATP ratio increased at both periods. Allopurinol pretreatment (40 mg kg(-1) iv) maintained higher ATP levels during the ischaemia and inhibited the MDA formation during the reperfusion and decreased the MDA/ATP ratio at both periods. Our findings demonstrate that allopurinol exerts a biphasic protective action by preserving tissue ATP and by inhibiting lipid peroxidation during ischaemia and the reperfusion period, respectively. These findings suggest the selective involvement of two protective mechanisms in the different periods of renal ischaemia-reperfusion injury. The MDA/ATP ratio could be a useful parameter for monitoring these protective actions of allopurinol simultaneously.

The beneficial effect of 2'-deoxycoformycin in renal ischemia-reperfusion is mediated both by preservation of tissue ATP and inhibition of lipid peroxidation.

Renal ischemia injures the renal tubular cell by disrupting the vital cellular metabolic machinery. Further cell damage is caused when the blood flow is restored by oxygen free radicals that are generated from xanthine oxidase. Oxygen radicals cause lipid peroxidation of cell and organelle membranes, disrupting the structural integrity and capacity for cell transport and energy metabolism. In the present study, the possible therapeutic usefulness of the adenosine deaminase inhibitor, 2'-deoxycoformycin (DCF), during renal ischemia and reperfusion injury was investigated. The effects of DCF on renal malondialdehyde (MDA) and ATP levels were studied after 45 min ischemia and 15 min subsequent reperfusion in rat kidneys. MDA levels remained unchanged during ischemia, but increased after the subsequent reperfusion. DCF pretreatment (2.0 mg/kg i.m.) decreased MDA and increased ATP levels during the ischemia-reperfusion period. DCF exerts a dual protective action by facilitating purine salvage for ATP synthesis and inhibiting oxygen radical-induced lipid peroxidation. These results suggest that DCF therapy could be beneficial in the treatment of ischemia-reperfusion renal injuries.

Effect of vitamin E on adriamycin- induced nephrotoxicity at the ultrastructural level in guinea pigs.

It is known that Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in several organs. In this study, we have established that vitamin E has some beneficial effects on the kidney by protecting it from some of the toxicity induced by Adriamycin. A study was carried out which comprised one control group and two experimental groups of guinea pigs. In the experiment Adriamycin was administered either alone (group II) or together with vitamin E (group III). The results of groups II and III were compared with controls (group I). The kidneys were subsequently removed and examined by routine electron microscopic techniques. We found that vitamin E administered together with Adriamycin could reverse some of the degenerative changes caused by Adriamycin.

The effect of different doses of epidermal growth factor on liver ornithine decarboxylase and Na-K ATPase activities in newborn rats.

1. Ornithine decarboxylase and Na-K ATPase activities were studied in rat livers that were treated with different doses of epidermal growth factor (EGF). 2. The ornithine decarboxylase activities were studied with spectrophotometry, and results were expressed as micromoles of putrescine per hour per milligram of protein. Na-K ATPase activities were studied on the basis of the principle of measuring the amount of inorganic phosphates released by the hydrolysis of ATP, and the results were expressed as micromoles of inorganic phosphate per hour per milligram of protein. 3. When compared with the controls, although the Na-K ATPase activities were decreased at low doses of EGF, their activities were found to be increased at high doses of EGF. On the other hand, there was a positive correlation between ornithine decarboxylase activities and EGF doses. 4. The results of this study suggest that, whereas the decrease in Na-K ATPase activities at low doses of EGF can be due to the utilization of the enzyme, the increase in Na-K ATPase activities at high doses of EGF can be attributed to its enhanced synthesis.

The dose-dependent effects of L-carnitine in myocardial protection in normothermic ischemia.

L-Carnitine has been shown to improve the post-ischemic recovery of myocardial function and metabolic measurements that are reduced in the course of ischemia and reperfusion of the heart. In this study we used 40 male guinea-pigs in order to determine if the effect of L-carnitine which is used in the protection of the post-ischemic reperfused heart, is dose-dependent or not. All harvested hearts were perfused for 30 min on modified Langendorf apparatus with oxygenized Krebs-Henseleit solution. After this period, in (n = 10), 5 mmol and 10 mmol (group B, n = 10) of L-carnitine were added into a Krebs-Henseleit solution. After 20 min, perfusion was complete and the hearts were then exposed to normothermic ischemia for 20 minutes. Following the ischemia, hearts were reperfused with the same solutions for 30 min. In group C (n = 10), 10 mmol of L-carnitine was added into the solution at the post-ischemic reperfusion step. In the control group, the same procedures were performed without using L-carnitine. Matching was done according to the contractile force of the heart rate and the levels of malondialdehyde and adenosine deaminase. When 10 mmol L-carnitine was added into the perfusion solutions at the pre-ischemic period, the best results were obtained and myocardial damage was much less than the control group. The protective effects of L-carnitine in normothermic ischemia is dose-dependent and it must be given at the pre-ischemic period.

Corneal aldehyde dehydrogenase and glutathione S-transferase activity after excimer laser keratectomy in guinea pigs.

BACKGROUND: The free radical balance of the eye may be changed by excimer laser keratectomy. Previous studies have demonstrated that excimer laser keratectomy increases the corneal temperature, decreases the superoxide dismutase activity of the aqueous, and induces lipid peroxidation in the superficial corneal stroma. Aldehyde dehydrogenase (ALDH) and glutathione S-transferase (GST) are known to play an important role in corneal metabolism, particularly in detoxification of aldehydes, which are generated from free radical reactions. METHODS: In three groups of guinea pigs mechanical corneal de-epithelialisation was performed in group I, superficial corneal photoablation in group II, and deep corneal photoablation in group III, and the corneal ALDH and GST activities measured after 48 hours. RESULTS: The mean ALDH and GST activities of group I and II showed no differences compared with the controls (p > 0.05). The corneal ALDH activities were found to be significantly decreased (p < 0.05) and GST activities increased (p < 0.05) in group III. CONCLUSION: These results suggest that excimer laser treatment of high myopia may change the ALDH and GST activities, metabolism, and free radical balance of the cornea.

Comparison of consequent small bowel anastomoses after transient ischemia: an experimental study in rats.

BACKGROUND/PURPOSE: The role of ischemia/reperfusion (I/R) damage on intestinal anastomotic healing remains to be precisely determined. The objective of this study was to investigate healing of small bowel anastomoses performed at different times after transient ischemia. METHODS: Thirty male Wistar-Albino rats were investigated in five groups (four study and one control). Under general anesthesia, the superior mesenteric artery (SMA) was occluded for 40 minutes in the study rats. Biopsy specimens, to document I/R histopathology, were obtained before small intestinal anastomoses at 20 minutes (group 1), 90 minutes (group 2), 6 hours (group 3), and 24 hours (group 4) after reperfusion. In a control group, biopsy and intestinal anastomoses were performed after SMA dissection without occlusion. The rats were relaparotomized on the fifth day to determine in situ bursting pressures and to obtain specimens for hydroxyproline content and histopathologic evaluation. RESULTS: Hydroxyproline content and bursting pressures were compared statistically with Mann-Whitney U test. Although there was no statistical difference between the control group and group 1, there were significant differences (P < .05) between groups 2, 3, and 4, with both parameters decreasing as the duration after reperfusion increased. CONCLUSION: Anastomosis are less likely to leak when performed sooner rather than later after an ischemia/reperfusion event.

Pentoxifylline inhibits overflow and reduces intestinal reperfusion injury.

The aim of this study was to determine the effects of pentoxifylline (Ptx) in reperfusion injury of the small bowel as a leukocyte stabilizer, free radical scavenger, and microcirculatory regulator. Ninety-six male Sprague-Dawley rats were used to determine the biochemical, histopathologic and blood flow changes of the reperfused small intestines after 30 minutes of a warm ischemic insult. Animals were divided into six groups: Sham (S), sham plus Ptx (SP), ischemia (I), ischemia plus Ptx (IP), reperfusion (R), and reperfusion plus Ptx (RP). Pentoxifylline was administered intraperitoneally at a dose of 50 mg/kg 15 minutes before ischemia. The superior mesenteric artery (SMA) was occluded distal to the right colic artery and collateral arcades were ligated as described by Megison. Sixty of the 96 rats (n = 10) were used to determine histopathologic changes, malondialdehyde (MDA), and myeloperoxidase (MPO) levels in tissue. Mucosal lesions were graded on a scale from 0 to 5 as described by Chiu. MDA and MPO levels of the intestinal mucosa were assayed to reflect the free radical formation and neutrophil sequestration, respectively. Thirty-six rats (n = 6) were used to measure blood flow changes of the intestine using 133Xe clearance technique. All data were presented as the mean values plus or minus the standard error of the means (means +/- sem). Although in the R group, mucosal injury score, blood flow, MPO, and MDA levels were higher significantly from the other groups (P < .05), in the RP group blood flow, MPO, and MDA levels were significantly decreased to the basal values (P < .05). Mucosal injury score of the RP group were lower than the reperfusion group but higher than the normal (P < .05). The authors conclude that pentoxifylline pretreatment before reperfusion stabilizes blood flow, decreases MPO and MDA levels to the normal, and attenuates but not completely prevents mucosal damage.

The effect of 2-chloroadenosine on lipid peroxide level during experimental cerebral ischemia-reperfusion in gerbils.

Oxygen free radicals may be implicated in the pathogenesis of ischemia-reperfusion damage. It is known that 2-chloroadenosine (2-CADO) has neuromodulatory effects and prevents the neuronal damage seen in the period of postischemia reperfusion. However, direct effects of 2-CADO on lipid peroxidation have not been investigated previously. The attack on the cell membrane by free radicals leads to lipid peroxidation, which can be assayed by the malondialdehyde (MDA) level. The aim of this study was to determine the effect of 2-CADO therapy on lipid peroxidation in experimental forebrain ischemia and postischemia reperfusion in Mongolian gerbils. Cerebral ischemia was induced by a bilateral 30-mm occlusion of the common carotid arteries. 2-Chloroadenosine (0.6 mg/kg, IV) was administered 5 min subsequent to ischemia. Ischemia was followed by reperfusion for 30 min. The MDA level was measured by the thiobarbituric acid (TBA) test. Bilateral carotid artery occlusion for 30 min in gerbils resulted in no significant change in MDA level in the brain. The MDA level was higher in postischemia reperfusion than in the ischemic group. 2-Chloroadenosine treatment did not change the MDA level in the ischemic period. However, the MDA level recovered significantly upon 2-CADO therapy during reperfusion following ischemia. These results suggest that 2-CADO may offer some degree of protection against oxidative stress in cerebral ischemia-reperfusion damage.

Influence of pulsed electromagnetic fields on healing of experimental colonic anastomosis.

PURPOSE: The study investigated the influence of pulsed electromagnetic fields (PEMFs) on the mechanical strength and collagen content of uncomplicated colonic anastomosis in rats. METHODS: A standardized left colonic resection was performed 3 cm above the peritoneal reflection, and end-to-end anastomosis was constructed with eight interrupted inverting sutures. Beginning immediately after surgery, randomly assigned groups were exposed to one of the following: 1) 100 Hz (frequency), 1 mT (intensity) PEMFs with 16-hour on/8-hour off cycles (n = 8); 2) 100 Hz, 2 mT PEMFs with 16-hour on/8-hour off cycles (n = 8); 3) 100 Hz, 1 mT PEMFs with 6-hour on/6-hour off cycles (n = 6), whereas the control group (n = 10) received no PEMFs. Relaparatomy was performed at 72 hours postoperatively, and the bursting pressure of the anastomotic segment was recorded in situ. The hydroxyproline contents of the anastomotic and adjacent perianastomotic segments of equal lengths were determined. RESULTS: Mean bursting pressure values of the groups that received 100 Hz, 1 or 2 mT PEMFs with 16-hour on/8-hour off cycles (90.88 +/- 19.13 and 83.88 +/- 7.08 mmHg, respectively) were significantly higher than those of the control group (61.66 +/- 10.6 mmHg) and the group with 6-hour on/6-hour off cycles (64.83 +/- 7.36 mmHg; P < 0.05 for all comparisons). Hydroxyproline contents of the anastomotic and perianastomotic segments were consistently higher in the 16-hour on/8-hour off PEMF groups, compared with those of the corresponding segments of the control group. CONCLUSIONS: PEMFs applied externally to unrestrained rats within a "window of PEMF parameters" provided a significant gain in the mechanical strength of the colonic anastomosis, at least 72 hours post-operatively. Associated relative increases in the hydroxyproline contents of the (peri)anastomotic colonic segments suggest that an altered collagen metabolism might contribute to this enhancement of the anastomotic repair. Further investigations based on these preliminary data and the definition of the exact measures regarding the effects of PEMFs on biologic systems, in general, may lead to an efficient and new adjunctive modality in colorectal surgery.