Caloric restriction improves the redox homeostasis in the aging male rat heart even when started in middle-adulthood and when the body weight is stable.

Evidence indicates that maintenance of redox homeostasis is fundamental for cellular longevity. Caloric-restriction (CR) is said to decrease the formation of oxidatively modified cellular macromolecules and improve health. On the other hand, some studies indicate that many CR studies are flawed, because ad libitum fed rats are not well-controlled. Thus, it is claimed that purported beneficial effects of CR could be not due to real CR effect, but due to control animals going obese. Also, it remains to be elucidated whether effects of CR could be observed even when CR is started in mid-adulthood. Male Sprague-Dawley rats were grouped as: non-CR 6-month-old rats (n = 7), 24-month-old rats subjected to 40% CR for 6 months between 18th and 24th months (n = 8), and non-CR 24-month-old animals (n = 8). We investigated 16 previously validated biomarkers of macromolecular redox homeostasis, ranging from protein and lipid oxidation to glycation and antioxidative capacity. In the present study, the protein, lipid and antioxidant capacity redox homeostasis biomarkers overwhelmingly indicate that, CR, even though not started very early in adulthood, could still offer potential therapeutic effects and it could significantly improve various redox homeostasis biomarkers associated with disease reliably in the heart tissue of aging male Sprague-Dawley rats. Therefore, the effects of CR likely operate through similar mechanisms throughout adulthood and CR seems to have real ameliorative effects on organisms that are not due to confounding factors that come from ad libitum fed rats.

Comparison of the metabolic and antioxidant effects of diltiazem and vitamin E on streptozotocin-diabetic rats.

In this study, solitary and combined effects of vitamin E and the calcium-channel blocker diltiazem were investigated in streptozotocin (STZ)-induced diabetic rats. Thirty male Wistar albino rats, weighing approximately 200 g were used. Diabetes mellitus was induced by a single intravenous injection of STZ at a dose of 65 mg/kg body weight. Five experimental groups were established as STZ-diabetic, STZ-diabetic + vitamin E, STZ-diabetic + diltiazem and STZ-diabetic + vitamin E + diltiazem. Vitamin E was injected intraperitoneally three times a week at a dose of 500 mg/kg body weight. Diltiazem was given orally every day at a dose of 25 mg/kg body weight. At the end of the study (10 weeks) blood glucose levels of diabetic rats, which had received vitamin E and diltiazem, had significantly decreased when compared with untreated diabetic rats (P < 0.02). Similarly, HbA1c levels had significantly decreased in diabetic rats which had received vitamin E (P < 0.05), diltiazem (P < 0.01) and vitamin E + diltiazem (P < 0.02) when compared with untreated diabetic rats. Liver glutathione levels of diabetic rats, which had received vitamin E (P < 0.01) and vitamin E + diltiazem (P < 0.05) had significantly increased when compared with untreated diabetic rats. Liver lipid peroxide levels had significantly decreased in diabetic rats, which had received vitamin E (P < 0.001) and diltiazem (P < 0.01). With respect to their metabolic and antioxidant effects, vitamin E proved superior to diltiazem.

Time-level relationship for nitric oxide and the protective effects of aminoguanidine in experimental spinal cord injury.

BACKGROUND: The secondary injury process following spinal cord trauma has been shown to involve different mechanisms such as excessive release of excitatory amino-acids, and induction of free radical induced lipid peroxidation. In this experimental study, the time-level relationship of the nitric oxide and the neuroprotective effects of aminoguanidine were investigated in a rat spinal cord trauma model. METHODS: The experiments were performed on 63 Wistar albino rats divided into three groups; sham-operated control (Group 1), trauma created control (Group 2) and aminoguanidine group (Group 3). In groups 2 and 3, spinal cord trauma was produced at thoracic level by using weight the drop technique (at a severity of 50 gr-cm). After the trauma, the rats in Group 3, received an intraperitoneal injection of 100 mg/kg aminoquanidine twice a day for 3 days. The effects of the injury and the efficacy of aminoguanidine were determined based on biochemical parameters (lipid peroxidation and nitric oxide levels in tissue), and on light microscopy findings in cord tissue collected at different times post-injury. Biochemical parameters were performed one hour, three and five days after injury. Functional recovery was assessed at 3, and 5 days after cord trauma with the inclined-plane technique and Tarlov's motor grading scale. FINDINGS: Although there was no statistically significant difference at the 1(st) hour, the values of the tissue nitric oxide in trauma created controls were 42% higher on the 3(rd) day and 40% higher on the 5(th) day when compared with those in sham controls. The levels of the tissue lipid peroxidation in trauma created controls were 88% higher at the 1(st) hour and 52.8% higher on the 5(th) day when compared with shame controls, but there was no meaningful difference on the 3(rd) day. In the trauma created control group, the mean motor function scores decreased to 1.16 +/- 0.40 and to 1 +/- 0 on the 3(rd) and 5(th) day, respectively. In this group the mean values of the inclined plane were 39.16 +/- 2.04 on the 3(rd) day and 37.91 +/- 1.02 on the 5(th) day. No statistically significant difference was observed in both tissue lipid peroxidation and nitric oxide levels for all time points between the aminoguanidine group and the sham-operated controls (p>0.01). The motor function scores were observed as 2.16 +/- 0.40 on the 3(rd) day and as 3 +/- 0 on the 5(th) day in aminoguanidine group. These values were significantly higher than the trauma created controls (p<0.01). Aminoguanidin treatment also improved the inclined plane performance of the rats; In this group, the mean values of the inclined plane scores were 44.58 +/- 2.92 and 52.91 +/- 1.88 on the 3(rd) and 5(th) days, respectively. These values were significantly higher than the trauma created controls (p<0.01). INTERPRETATION: This study shows that the nitric oxide level does not increase in the spinal cord tissue during the first hour after the spinal cord trauma. It increases significantly in the spinal cord tissue not only three days but also five days following the trauma. Aminoguanidine treatment, which is started just after the trauma, can prevent both the nitric oxide production and lipid peroxidation in spinal cord tissue and it can improve the functional status of the animals. In this respect, aminoguanidine may have a potential role in the treatment of acute spinal cord injury.

Total sialic acid levels decrease in the periventricular area of infantile rats with hydrocephalus.

OBJECT: Besides mechanical damage done by the enlarging ventricles, biochemical impairment in the periventricular tissue represents an important factor resulting from or contributing to the pathogenesis of hydrocephalus. In this study the changes in periventricular region total sialic acid levels in the early stage of experimentally induced hydrocephalus were evaluated. METHODS: Hydrocephalus was induced in 3-week-old rat pups by kaolin injection into the cisterna magna. Ten days after hydrocephalus induction rats were sacrificed and total sialic acid levels in the periventricular area were determined by the thiobarbituric acid method. CONCLUSION: Sialic acid, a vital component of brain gangliosides, which play an essential role in the transmission and storage of information in the brain, was found to be significantly decreased in the periventricular area of hydrocephalic infantile rats.

Is intestinal ischemia a risk of laparoscopy? An experimental study in rabbits.

BACKGROUND AND PURPOSE: In the literature, there are few reports documenting intra-abdominal organ necrosis following laparoscopic procedures. This experimental study was planned to investigate whether intestinal ischemia develops during laparoscopic procedures and if laparoscopy could cause intestinal necrosis. MATERIAL AND METHODS: Two experimental groups, each consisting of 10 adult New-Zealand rabbits, were used in this study. The first group comprised the study group which had pneumoperitoneum, the second group comprised the normal animals serving as the controls. A cervical tracheostomy was performed to achieve successful general anesthesia in both groups. In the study group, intraperitoneal CO2 insufflation was carried out and intraabdominal pressure (IAP) was adjusted so as not to exceed the arterial blood pressure. After 20 min high IAP period, the intraabdominal gas was aspirated. Five minutes later, samples of both small intestine and colon tissue were taken. In the control group, tissue samples were taken 25 min after anesthesia was achieved. Xanthine oxidase (XO) and malondialdehyde (MDA) levels were measured as indicators of intestinal ischemia and lipid peroxidation in the intestinal tissues. Statistical analysis was done to compare the XO and MDA levels of the small intestines and colons of both groups. RESULTS: The mean colonic XO levels were 1.323+/-1.17 and 0.217+/-0.27 (U/mg protein) in study and control groups, respectively. This difference was statistically significant (t = 2.60, p<0.05). The other comparisons with regard to XO and MDA levels were statistically not significant. CONCLUSION: Our results demonstrate that intraperitoneal CO2 insufflation in which intraabdominal pressure was adjusted to be lower than arterial blood pressure may affect oxygenization of the colon.

Evaluation of salivary sialic acid level and Cu-Zn superoxide dismutase activity in type 1 diabetes mellitus.

In this study, our aim was to determine whether or not type 1 diabetes mellitus affects salivary sialic acid level and SOD activity. For this purpose, unstimulated saliva specimen was collected. Saliva sialic acid level and SOD activity were measured by the methods of Warren and Sun, respectively. We found significantly decline in salivary sialic acid level and SOD activity. The decrease of salivary sialic acid level in type 1 diabetes may be due to changes in the activities of the enzymes taking part of in the synthesis and catabolism of sialic acid. The main reason for the decrease of salivary SOD activity may be increased glycation of the enzyme and/or deleterious effect of increased free oxygen radicals by glycated proteins on SOD activity in diabetes. We conclude the decline both in sialic acid and SOD in saliva may be a possible factor leading to oral complications of diabetes mellitus.

The effect of duration of compression on lipid peroxidation after experimental spinal cord injury.

The present study was performed to evaluate the effect of duration of acute spinal cord compression on tissue lipid peroxidation in rats. A clip compression method (1) was used to produce acute spinal cord injury. Rats were divided into 3 groups, each consisting of 10. At 1 hour after trauma all rats were sacrificed, and MDA content of the injured spinal cord segment was measured. The tissue MDA contents were 3.922 mumolMDA/gww in group 1 (control), 10.192 mumol MDA/gww in group 2 (30 seconds compression), and 12.147 mumolMDA/gww in group 3 (60 seconds compression). These results demonstrate that the length of duration of compression significantly enhances lipid peroxidation. Our study supported the view that persisting compression may cause progression of secondary mechanisms which may irreversibly eliminate any potential for recovery.

The effect of epidural cooling on lipid peroxidation after experimental spinal cord injury.

STUDY DESIGN: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. OBJECTIVES: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective effects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. SETTING: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. METHODS: Twenty-five female Wistar Albino rats were used. There were five rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining five rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a flow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacrificed and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). RESULTS: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group I (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/gww in group 3 (epidural cooling), the differences being statistically significant. CONCLUSION: The results indicated that epidural cooling of traumatized spinal cord is effective in preventing secondary damage due to the peroxidation of lipid membranes.

Effect of nimodipine and N-acetylcysteine on lipid peroxidation after experimental spinal cord injury.

The effectiveness of nimodipine and N-acetylcysteine in experimental spinal cord injury was evaluated by measuring tissue lipid peroxidation levels of the damaged spinal cords 1 hour after the injury We used the clip compression method to produce acute spinal cord injury in 40 female Sprague-Dawley rats were used. The rats were divided into four groups of 10 each. Lipid peroxidation was assessed by measuring the tissue content of malonil dialdehyde (MDA). In group 3, nimodipine, and in group 4, N-acetylcysteine, was administered i.p. as a single dose immediately after the injury. The rats were sacrificed 1 hour after clip application. The tissue mean MDA content was 3,992 micromol MDA/gww in group 1 (sham operated), 10,192 micromol MDA/gww in group 2 (trauma), 10,449 micromol MDA/gww in group 3 (nimodipine treatment) and 9,009 micromol MDA/gww in group 4 (N-acetylcysteine treatment). These results demonstrated that a single dose of nimodipine and N-acetylcysteine had no effect on peroxidation of lipid membranes in the early period of experimental spinal cord injury.

Evaluation of lipid peroxidation and total antioxidant status in plasma of rats following thermal injury.

Thermal injury initiates systemic inflammatory reactions producing burn toxins, an inflammatory response, oxygen radicals and finally peroxidation. The relationship between the amount of products of oxidative metabolism and natural scavengers of free radicals determines the outcome of local and distant tissue damage, and further organ failure in burn injury. To determine the relationship between the level of total natural scavengers of the body, the place of superoxide dismutase in this capacity, and its relation with lipid peroxidation, malondialdehyde, superoxide dismutase levels and total antioxidant status were measured in plasma. Animals were subjected to 30 per cent full thickness body surface area burn, and their blood was collected at 24 h postburn. Plasma malondialdehyde levels were significantly elevated above the level of controls (P < 0.02). Burn injury caused a remarkable decrease in superoxide dismutase (45 per cent decrease, P < 0.0001) and total antioxidant status (14 per cent decrease, P < 0.01) when compared to control.

Changes in the activity of antioxidant enzymes (SOD, GPX, CAT) after experimental spinal cord injury.

We determined time dependent changes in the levels of the antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) at 1, 4 and 24 hours after standardized reversible spinal cord injury in rats. In each segment (rostral, lesion, caudal) enzyme activities at 1, 4 and 24 hours were not significantly different. Without time limitation we have found that SOD and GPx activities were not significantly different (p > 0.05), but CAT activity was significantly high (p = 0.008) in the lesion segment than the rostral and caudal segment. According to our results we suggest that one of the main reason for tissue damage during such a spinal cord trauma model may be neither H2O2 nor H2O2 derived radicals.

Xanthine oxidase levels in human brain tumors.

Xanthine oxidase is most recognized for its role as the rate-limiting enzyme in nucleic acid degradation through which all purines are channelled for terminal oxidation. The enzyme serves as a source of oxygen-derived free radicals which induce both cellular injury and edema as well as changes in vascular permeability. In the study we compared xanthine oxidase levels of human brain tumors with normal brain tissues. Statistical evaluation of our results shows significantly higher xanthine oxidase levels in tumoral brain tissues. However, xanthine oxidase has not any significance for the differentiation of tumor types among each others. The oncotypes studied were meningioma and astrocytoma.

Leucocyte superoxide dismutase levels in acute and chronic leukemias.

Superoxide dismutase "SOD" enzyme levels in leucocytes of patients with acute and chronic leukemia, were measured by using Misra and Fridovich's epinephrine method. In all types of leukemia, the SOD levels were found to be significantly higher than normals. However, these levels decreased to normal in remission. No relationship was found between the SOD level and types of leukemia. The absence of relationship between the increase in SOD level and various clinical parameters suggests that this increase is the result of a disturbed gene expression in the stem cells. Hence it is of interest to ascertain the effect of the chemotherapy leading to the normalization of the SOD levels.