Therapeutic and prophylactic role of vitamin D and curcumin in acetic acid-induced acute ulcerative colitis model.

Ulcerative Colitis (UC) is a disease that negatively affects quality of life and is associated with sustained oxidative stress, inflammation and intestinal permeability. Vitamin D and Curcumin; It has pharmacological properties beneficial to health, including antioxidant and anti-inflammatory properties. Our study investigates the role of Vitamin D and Curcumin in acetic acid-induced acute colitis model. To investigate the effect of Vitamin D and Curcumin, Wistar-albino rats were given 0.4 mcg/kg Vitamin D (Post-Vit D, Pre-Vit D) and 200 mg/kg Curcumin (Post-Cur, Pre-Cur) for 7 days and acetic acid was injected into all rats except the control group. Our results; colon tissue TNF-α, IL-1ß, IL-6, IFN-γ and MPO levels were found significantly higher and Occludin levels were found significantly lower in the colitis group compared to the control group (p < 0.05). TNF-α and IFN-γ levels decreased and Occludin levels increased in colon tissue of Post-Vit D group compared to colitis group (p < 0.05). IL-1ß, IL-6 and IFN-γ levels were decreased in colon tissue of Post-Cur and Pre-Cur groups (p < 0.05). MPO levels in colon tissue decreased in all treatment groups (p < 0.05). Vitamin D and Curcumin treatment significantly reduced inflammation and restored the normal histoarchitecture of the colon. From the present study findings, we can conclude that Vitamin D and Curcumin protect the colon from acetic acid toxicity with their antioxidant and anti-inflammatory potential.Brief synopsis: In this study; distal colon, distal ileum, jejunum and serum physiopathology in colitis induced by acetic acid and intestinal permeability were investigated. The roles of vitamin D and curcumin in this process were evaluated.

Protective effects of Ficus carica seed oil on ischemia and reperfusion injury in a rat model of acute mesenteric ischemia.

BACKGROUND: The increase in free oxygen radicals and proinflammatory cytokines in the ischemia-reperfusion injury caused by acute mesenteric ischemia are the key responsibilities of intestinal histopathological alterations. It has been reported that Ficus carica and its various parts contain antioxidant and anti-inflammatory compounds recently. Thus, in the present study, we aimed to investigate how Ficus carica seed oil affects intestinal ischemia-reperfusion injury in a rat model. METHODS: In this study, 50 male Wistar albino rats were randomly divided into five equal groups. Negative control (NC), sham-operated (Sham), ischemia and reperfusion (IR), 3 ml/kg/day Ficus carica seed oil (FC3), 6 ml/kg/day Ficus carica seed oil (FC6). IR, FC3 and FC6 groups underwent ischemia and reperfusion procedure for 45+120 min. Only abdominal midline laparotomy was performed in the Sham group for 165 minutes. RESULTS: Tissue levels of TNFα and IL-1ß, which were proinflammatory cytokines, were significantly reduced in the FC6 group than the IR group (p<0.05). In FC3 and FC6 groups, the tissue MPO and MDA enzyme levels were significantly lower than the IR group, but there was a significantly greater decrease in the FC6 group than the FC3 group (p<0.05). SOD and CAT enzymes and reduced glutathione levels of FC3 and FC6 groups were significantly lower than IR group (p<0.05); however, there was no statistically significant difference between the FC3 and FC6 groups. FC3 and FC6 groups were histopathologically graded statistically lower than the IR group, and the FC6 group showed a significant decrease than the FC3 group (p<0.05). CONCLUSION: Oral administration of fig seed oil may reverse biochemical and histopathological findings resulting from ischemia-reperfusion injury in an experimental model of acute mesenteric ischemia in rats, probably because of its antioxidant and anti-inflammatory compounds.

Effect of experimentally induced hypothyroidism during gestation period on activity dependent neurotrophic factor (ADNF) in newborn rat brain tissue.

Purpose The aim of the study was to evaluate the effects of prenatal hypothyroidism on neonatal rats by the way of activity-dependent neuroprotective factor (ADNF) expression. Methods Twenty-one Wistar albino neonatal rats were divided into two subgroups; a control group and neonatal rats with experimental maternal hypothyroidism. Hypothyroidism was induced by using propylthiouracil (PTU). Neonatal rats obtained PTU from breast milk continuously for 1 week after birth. The rats from the control group were fed only normal feed and water. After birth, body weight and blood thyroid hormone levels were tested. Glial fibrillary acidic protein (GFAP), Slug, Numb, Notch-1 and ADNF antibodies were used for immunohistochemical analysis. Real-time polymerase chain reaction (RT-PCR) and Western blotting analyses were used to evaluate ADNF gene expression levels from 1-week-old rat's brain. Results There was no difference between the two groups for birth weights. The thyroxine (T4) level from the experimental group was <0.4 ng/mL, and it was 0.8 ng/mL for the control group. It was shown that, the results from the experimental group samples had significantly lower ADNF mRNA levels than control group (p < 0.05). The increase from GFAP and Numb expression and decrease from Slug expression were shown in the experimental group. Local differences were identified for ADNF and a decrease was shown in both sides of brain. There was no difference for Notch-1 expression for both groups. Conclusion In this study, decreasing ADNF expression might contribute to developing neurological problems in congenital hypothyroidism.

The Effect of Congenital and Postnatal Hypothyroidism on Depression-Like Behaviors in Juvenile Rats.

OBJECTIVE: The aim of this study was to investigate depression-like behaviors of juvenile rats with congenital and postnatal hypothyroidism. METHODS: Twenty-seven newborn rat pups were used. First, 6-month-old Wistar Albino female rats were impregnated. Methimazole (0.025% wt/vol) was given to dam rats from the first day of pregnancy until postnatal 21 days (P21) to generate pups with congenital hypothyroidism (n=8), whereas in the postnatal hypothyroidism group (n=10), methimazole was given from P0 to P21. In the control group (n=9), dam rats were fed ad libitum and normal tap water. Offspring were fed with breast milk from their mothers. The behavioral parameters were measured with the juvenile forced swimming test (JFST). The procedure of JFST consisted of two sessions in two consecutive days: the 15-minute pre-test on day 1 and the 5-minute test on day 2. RESULTS: Increased immobility and decreased climbing duration were observed in both congenital and postnatal hypothyroidism groups. Decreased swimming duration was detected in the postnatal hypothyroidism group. Both hypothyroidism groups had a lower body weight gain compared with the control group, while the congenital hypothyroidism group had the lowest body weight. CONCLUSION: Our results showed that hypothyroidism had negative effects on depression-like behavior as well as on growth and development. Both congenital and postnatal hypothyroidism caused an increase in immobility time in JFST. New studies are required to understand the differing results on depression-like behavior between congenital and postnatal hypothyroidism.

[Laryngeal effect of experimental postnatal hypothyroidism: do thyroid hormone receptors change?]. / Deneysel postnatal hipotiroidinin larenkse etkisi: Tiroid hormon reseptörleri degisiyor mu?

OBJECTIVES: In this study, we aimed to investigate the laryngeal histopathological alterations and thyroid hormone receptors in rats with experimentally-induced postnatal hypothyroidism. MATERIALS AND METHODS: In this prospective, randomized study, pregnant Wistar albino rats were followed and newborn 20 Wistar albino rat pups were included in the study. The pups were randomly divided into two groups: In group 1 (methimazole (MMI)-induced hypothyroidism group), the mothers and pups were given MMI added water up to 90th day, as the pups were fed with breast milk for 19 to 22 days. In group 2 (control group), the mothers and pups were fed with MMI-free water up to 90th days. When the pups were 90 days of age, they were decapitated and their larynx was removed. Their larynx was evaluated for edema, inflammation, goblet cells, and thyroid hormone receptors (TR-α, TR-ß). RESULTS: Nine larynx samples for group 1 and eight for group 2 were studied. There was a significant difference in inflammation between the groups with slightly lower in the hypothyroidism group (p=0.009). The TR-α, TR-ß, and edema were significantly higher in the hypothyroidism group (p=0.002, p=0.029, p=0.029). There was no significant difference in the Goblet cells between the groups (p=0.637). CONCLUSION: Histopathologically increased laryngeal edema and increased thyroid hormone receptors were found, shedding light on the mechanism of voice changes in hypothyroidism.

Do prenatal and postnatal hypothyroidism affect the craniofacial structure?: An experimental study.

OBJECTIVE: To investigate the effect of experimental prenatal and postnatal hypothyroidism (HT) on the craniofacial structure in rats. MATERIALS AND METHODS: Female Wistar albino rats were mated with males for fertilization. Pregnant rats were divided into three groups. Group 1 (methimazole [MMI]-induced prenatal hypothyroidism group) mother rats were given MMI water during and after pregnancy. Group 2 (MMI-induced postnatal hypothyroidism group) mother rats were given MMI water after pregnancy. After the breast-feeding period, group 1 and 2 rat pups received the same water as their lactating mothers drank. Group 3 (control group) pregnant rats and rat pups were given normal tap water. When the rat pups were 90 days of age, lateral cephalometric and posteroanterior films were taken under anesthesia. RESULTS: Posteroanterior radiographs revealed that palatal, cranial, bizygomatic arch, and bigonial width measurements were significantly shorter in prenatal HT and postnatal HT groups compared to the control group (P < .001). Intragroup comparisons in lateral cephalometric radiographs showed that, nearly all of the comparisons were statistically significant (P < .05), with the exception of the Co-Gn, E-Pg/S-Gn measurements between the prenatal and postnatal HT groups. CONCLUSIONS: Sagittal and transverse measurements showed that untreated HT has detrimental effects on the growth of the maxilla and mandible.

The effect of methimazole-induced postnatal hypothyroidism on the retinal maturation and on the Sirtuin 2 level.

PURPOSE: To investigate the effect of methimazole-induced postnatal hypothyroidism on the retinal maturation and to study Sirtuin 2 (SIRT2) level in the hypothyroidic rat retina. METHODS: Twenty newborn Wistar albino rat pups were used in this prospective, randomized study. Wistar albino rats, weight 250-300 g, were impregnated (without addition of any drug) and were fed normally. Rat pups were randomly divided into two groups and were fed with breast milk. After weaning till they were 90 days of age, rat pups received the same water as their lactating mothers drank. Group 1 (methimazole (MMI)-induced hypothyroidy group), rats were given MMI-water, whereas, in Group 2, normal tap water. When the pups were 90 days of age, 20 rat pups were decapitated and the eyes were isolated. Eyes were investigated using histological, histomorphometric and immunohistochemistrical techniques. RESULTS: No histological difference was seen between the groups stained with hematoxylin and eosin. In both groups the retinal layer structures and cells were observed as normal. The examples in the groups had a normal distribution for retinal thickness (pixel) measure. The mean value (mean ± std. deviation) was 554.7 ± 228.4 in the control group and 494.7 ± 129.4 in the hypothyroidy group. There was no significance between the groups in terms of retinal thickness (p = 0.231). However, immunohistochemistry revealed that SIRT2 was weaker stained in the ganglion cell layer and visual cell layer in the hypothyroidy group compared to the control group. CONCLUSION: Postnatal hypothyroidism altered the retinal cytoarchitecture and layering which are regulated by thyroid hormones (THs) during retinal maturation in the postnatal period. THs may act by the induction of the SIRT family proteins or through their receptors. Postnatal screenings for THs levels are very important to provide normal retinal development.

Effects of (99m)Tc sestamibi on antioxidant defense system and lipid peroxidation in the heart of Sprague Dawley rats.

Nuclear medicine has been using radiopharmaceuticals for the diagnostic and therapeutic purposes of many diseases. Technetium-(99m) methoxyisobutylisonitrile ((99m)Tc sestamibi) is a lypophilic complex that has a positive-loaded isonitril group. Aim of the study is to investigate whether (99m)Tc sestamibi, which is one of the mostly used radiopharmaceuticals in nuclear medicine field, causes oxidative damage or not in rats' heart after an injection. A total of 16 male Sprague Dawley rats were randomly divided into two groups: group I: (99m)Tc sestamibi group, (99m)Tc sestamibi administered intravenously with the dose of 25MBq; group II: control group, one dose of isotonic sodium chloride was administered intravenous with the same volume as (99m)Tc sestamibi group. Malondialdehyde (MDA) and total oxidant status (TOS) were used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and total antioxidant status (TAS) activities were studied to evaluate the changes in the antioxidant status. In the (99m)Tc sestamibi group (group I), animals treated with (99m)Tc sestamibi produced a significant decrease in the activities of antioxidant enzymes (SOD and CAT), while MDA level increased when compared with control group (group II) in myocardial tissue (p < 0.05). On the other hand, the GSH-Px activities were significantly increased in the (99m)Tc sestamibi-treated rats compared with the untreated rats (p < 0.05). There was no significant difference in the TAS and TOS levels of plasma.

The relationship between ghrelin and adiponectin levels in breast milk and infant serum and growth of infants during early postnatal life.

Ghrelin and adiponectin have been found in breast milk and are considered to take part in the regulation of growth and energy metabolism of infants. Our aims were to determine ghrelin and adiponectin levels in breast milk and serum samples of mothers and their infants, and to investigate the relationship between their levels and anthropometry of newborn infants during early postnatal life. Total and active ghrelin and adiponectin levels were studied in breast milk, and the serum samples of 25 healthy lactating women and their healthy fullterm infants were taken at the 1st and 4th months of life. Anthropometric measurements of infants were also performed during the study period. Breast milk and infant serum active ghrelin levels were found to be significantly increased at the 4th month of life compared with 1st month levels (p < 0.05). Maternal serum total ghrelin and infant serum adiponectin levels were found to be significantly reduced at the 4th month of life (p < 0.05). Breast milk active ghrelin levels were higher than the infant and maternal serum active ghrelin at the 1st and 4th months (p < 0.05). There was a negative significant correlation between the level of infant serum active ghrelin levels and BMI of infants at the 1st month. A positive significant correlation was found between the level of 1st month infant serum adiponectin levels and weight gain of infants during the study period. Fourth month infant serum adiponectin were also positively correlated with weight and BMI of infants at the 4th month and the weight gain during study period. There was a positive significant correlation between the level of 4th month breast milk active ghrelin and weight gain of infants during the study period. Ghrelin and adiponectin are involved in postnatal growth of infants. Ghrelin in breast milk also seems to be related to the growth of infants during early postnatal life. The sources of these peptides in breast milk are probably both maternal serum and breast tissue itself.

Ghrelin and adiponectin levels in colostrum, cord blood and maternal serum.

BACKGROUND: Ghrelin and adiponectin, which are considered to take part in the regulation of energy metabolism, have been found in breast milk and cord blood. The aims of this study were to determine ghrelin and adiponectin levels in colostrum, cord blood and maternal serum and to investigate the correlations between colostrum and cord blood levels of these peptides and the anthropometry of newborn infants and their mothers. METHODS: Total ghrelin (TGHR), free ghrelin (FGHR) and adiponectin levels were studied in colostrum and the serum samples of 25 healthy lactating women and the cord blood of their healthy full-term infants. RESULTS: No significant differences could be found among TGHR and adiponectin levels in colostrum, cord blood and maternal serum. The median FGHR level in colostrum was significantly higher than that of maternal serum and cord blood. The colostrum TGHR was negatively correlated with body mass index (BMI) and weight of the infants at birth. TGHR and FGHR levels in colostrum were found to be positively correlated with those of maternal TGHR and FGHR concentrations, respectively. Adiponectin levels in colostrum were not correlated with BMI or birthweight of the infants or BMI of the mothers. CONCLUSION: These findings suggest that the source of ghrelin in breast milk is probably both breast tissue itself and the serum of the mother. Ghrelin in colostrum seems to be related to the anthropometry of infants even at birth, unlike adiponectin.

The effect of the prenatal and post-natal long-term exposure to 50 Hz electric field on growth, pubertal development and IGF-1 levels in female Wistar rats.

To investigate prenatal and post-natal effects of extremely low frequency (ELF) electric field (EF) on growth and pubertal development, pregnant Wistar rats were randomly distributed among three groups. The pregnant rats of the prenatal group were exposed to 24-hour EF at 50 Hz EF 10 kV/min during pregnancy and their subsequent randomly selected female pups continued to be exposed until puberty. The post-natal group was unexposed to EF during pregnancy, but randomly selected female pups from this group were exposed to EF between delivery and puberty at the same doses and duration as the prenatal group. The third group was a sham-exposed group. The mean birth weight and weight gain of the pups during study period were found significantly reduced in prenatal group than post-natal and sham-exposed groups (p < 0.001). No difference could be found among the three groups for body weight at puberty (p > 0.05). The mean age at vaginal opening and estrous were significantly higher at prenatal group than post-natal and sham-exposed groups (p < 0.001). Serum insulin-like growth hormone-1 (IGF-1) levels were found significantly reduced in prenatal exposure group compared with the other two groups (p < 0.001). There was no difference for birth weight, weight gain, the mean age at vaginal opening and estrous and IGF-1 levels between post-natal and sham-exposed groups (p > 0.05). There was also no difference for FSH, LH and E2 levels at puberty among the three groups (p > 0.05). Histological examination revealed that both the prenatal and post-natal groups had the evidence of tissue damage on hypothalamus, pituitary gland and ovaries. In conclusion, early beginning of prenatal exposure of rats to 24 hours 50 Hz EF at 10 kV/m until puberty without magnetic field (MF) resulted in growth restriction, delayed puberty and reduced IGF-1 levels in female Wistar rats. These effects probably associated with direct toxic effects of EF on target organs. Post-natal exposure to EF at similar doses and duration seems to be less harmful on target organs. Post-natal exposure to EF at similar doses and duration seems to be less harmful.

Influence of electromagnetic fields on bone fracture in rats: role of CAPE.

OBJECTIVE: To study the effects of radiation emitted by mobile phones on bone strength and caffeic acid phenethyl ester (CAPE) on the changes induced by radiation. METHODS: Forty-eight Sprague-Dawley rats were divided into five groups. Rats in the control group (first group) were left within the experimental setup for 30 min/day for 28 days without radiation exposure. Nine hundred MHz radiation group was broke down into 2 subgroups (group 1/2). Both subgroups were exposed to radiation for 28 days (30 min/day). The next group was also divided into 2 subgroups (group 3/4). Each was exposed to 1800 MHz of radiation for 28 days (30 min/day). The third and fifth groups were also treated with CAPE for 28 days. Treatment groups received ip caffeic acid phenethyl ester (10 micromol/kg per day) before radiation session. Bone fracture was analyzed. RESULTS: Breaking force, bending strength, and total fracture energy decreased in the irradiated groups but increased in the treatment groups. CONCLUSION: Radiation and CAPE can significantly improve bone.

Chlorpyrifos increases the levels of hippocampal NMDA receptor subunits NR2A and NR2B in juvenile and adult rats.

The present study investigated the effect of chlorpyrifos on NMDA receptor subunits NR2A and NR2B in juvenile and adult rats. Chlorpyrifos was administered with the dose of 40 and 70 mg/kg to juvenile and adult rats, respectively. Chlorpyrifos significantly inhibited the AChE activity in juvenile and adult rats (p < .05). NR2A and NR2B levels significantly increased in juvenile and adult rats by chlorpyrifos application (p < .05). Increased NR2A and NR2B levels may reflect increased glutaminergic activity, consequently neuronal damage. In the case of neuronal damage, learning and memory could be affected negatively even though NR2A and NR2B increased.

DEXA analysis on the bones of rats exposed in utero and neonatally to static and 50 Hz electric fields.

Effects of the electromagnetic fields on living bodies, bones in particular, are among the relevant issues of contemporary life. In this study, we report the influences of 50 Hz and 0 Hz (static) electric fields (EF), on intact rat bones, as evaluated by dual energy X-ray absorbtion (DEXA) measurements on bone content and density when these animals (n = 27) are continuously exposed in utero and neonatally to EFs (10 kV/m) 14 days before and 14 days after their birth, for 28 days in total. Differences between 50 Hz EF and static EF groups are found to be significant (95% confidence level) for total bone mineral content (BMC), TBMC (P = .002). Differences between 50 Hz and control groups are found to be significant for total bone mineral density (BMD), TBMD (P = .002), lumbar BMC, LBMC (P = .023), and TBMC (P = .001). Differences between static EF and control groups are found to be significant for femoral BMD, FBMD (P = .009), TBMD (P = .002), LBMC (P = .001), and TBMC (P = .001). Note that TBMC parameters are jointly significant for all differences between the three groups of test animals. These results have shown that both static and 50 Hz EFs influence the early development of rat bones. However, the influence of static EFs is more pronounced than that of the 50 Hz field.

The influence of continuous exposure to 50 Hz electric field on nerve regeneration in a rat peroneal nerve crush injury model.

The effect of power frequency electric field (EF) on nerve regeneration was investigated on a rat peroneal nerve crush injury model. The animals were assigned to three groups: 50 Hz EF and Static EF groups were exposed at 10 kV/m. The sham group was kept in the same setting without any EF applications. EF was uninterruptedly applied for 21 days postoperatively. Repeated measures analysis of daily walking tracks during EF exposure demonstrated lower toe spread recovery (TSR) in the 50 Hz EF group. Significant difference across the groups was found only at days 7, 8, 12, 16, 17, 20, and 21 when TSR was analyzed for each measurement time. Print length recovery and peroneal function index did not differ across the groups. Walking track parameters were found to recover to their baseline values by day 28 in all groups. Day 14 but not day 21 measurements revealed smaller nerve cross-sectional area, lower total regenerating axon area, and higher mean myelin debris area in 50 Hz EF group. Both day 14 and 21 measurements revealed higher total myelin debris area, lower EDL muscle weight, and lack of significant enlargement in nerve cross-section distal to the injury, compared to the normal counterpart in 50 Hz EF group. All differences were in keeping with lower rates of Wallerian degeneration and nerve regeneration in 50 Hz EF group. When walking track, histomorphometry and muscle weight are considered individually, their differences across the groups may appear to be subtle to derive a conclusion for a 50 Hz EF effect. However, their concordance with each other in direction of effect suggests that continuous 50 Hz EF exposure has a weak effect that is detrimental mostly to the rate of early nerve regeneration in this axonotmetic injury model. Recovery of walking tracks was not different between Static EF and Sham groups. This suggests that the surface charges that may indirectly affect walking behaviors of the rats, do not account for the lower recovery of TSR in 50 Hz EF group. Differences in nerve regeneration between 50 Hz EF and Static EF groups suggests that electric induction may be required for pure EF effects even though the estimated density of induced fields is not above the endogenous background level for the 50 Hz EF exposure in this study.

Endometrial apoptosis induced by a 900-MHz mobile phone: preventive effects of vitamins E and C.

Numerous reports have described the effects induced by an electromagnetic field (EMF) in various cellular systems. The purposes of this study were to examine oxidative stress that promotes production of reactive oxygen species induced by a 900-megahertz (MHz) mobile phone and the possible ameliorating effects of vitamins E and C on endometrial tissue against EMF-induced endometrial impairment and apoptosis in rats. Animals were randomly grouped as follows: (1) sham-operated control group (n=8), (2) 900 MHz EMF-exposed group (n=8; 30 min/d for 30 d), and (3) 900 MHz EMF-exposed group, treated with vitamins E and C (n=8; 50 mg/kg intramuscularly and 20 mg/kg body weight intraperitoneally before daily EMF exposure). Malondialdehyde (an index of lipid peroxidation) was used as a marker of oxidative stress-induced endometrial impairment; Bcl-2, Bax, caspase-3, and caspase-8 were assessed immunohistochemically. In this study, increased malondialdehyde levels in endometrial tissue and apoptosis illustrated the role of the oxidative mechanism induced by exposure to a 900-MHz mobile phone-like device and vitamins E and C; via free radical scavenging and antioxidant properties, oxidative tissue injury and apoptosis were ameliorated in rat endometrium. In conclusion, exposure to 900-MHz radiation emitted by mobile phones may cause endometrial apoptosis and oxidative stress, but treatment with vitamins E and C can diminish these changes and may have a beneficial effect in preventing endometrial changes in rats.

Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester.

Electromagnetic radiation (EMR) or radiofrequency fields of cellular mobile phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation, and by changing the antioxidant defense systems of human tissues, thus leading to oxidative stress. Mobile phones are used in close proximity to the heart, therefore 900 MHz EMR emitting mobile phones may be absorbed by the heart. Caffeic acid phenethyl ester (CAPE), one of the major components of honeybee propolis, was recently found to be a potent free radical scavenger and antioxidant, and is used in folk medicine. The aim of this study was to examine 900 MHz mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and the role of CAPE on myocardial tissue against possible oxidative damage in rats. Thirty rats were used in the study. Animals were randomly grouped as follows: sham-operated control group (N: 10) and experimental groups: (a) group II: 900 MHz EMR exposed group (N: 10); and (b) group III: 900 MHz EMR exposed+CAPE-treated group (N: 10). A 900 MHz EMR radiation was applied to groups II and III 30 min/day, for 10 days using an experimental exposure device. Malondialdehyde (MDA, an index of lipid peroxidation), and nitric oxide (NO, a marker of oxidative stress) were used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status. In the EMR exposed group, while tissue MDA and NO levels increased, SOD, CAT and GSH-Px activities were reduced. CAPE treatment in group III reversed these effects. In this study, the increased levels of MDA and NO and the decreased levels of myocardial SOD, CAT and GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced heart tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative heart injury. These results show that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative heart impairment in rats.

Active smoking causes oxidative stress and decreases blood melatonin levels.

Oxidative effects via free radical generation in smokers have been widely investigated. They cause lipid peroxidation, oxidation of proteins and damage to mainly lung and other tissues. In humans, antioxidative capacity of serum is related to antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and melatonin. The effect of cigarette smoking on plasma levels of melatonin and antioxidant enzymes has not been established together yet. Also, it may not be clear if melatonin levels are affected by smoking and melatonin has a protective effect on cigarette smoking-induced free radical damage. The aim of this study is to investigate the relationship between smoking and antioxidant capacity including melatonin, a powerful endogenous antioxidant, and antioxidant enzymes in teenage girls who are active smokers. Additionally, malondialdehyde (MDA) levels were determined in those who have smoked at least one packet a day for three or more years. MDA levels have been used as a convenient index of the lipid peroxidation-related oxidative damage of tissues. Twenty-one young female active smokers who study at the School of Nursing and 21 nonsmoking students (as controls) at the same school were included in the study. The activities of two principal antioxidant enzymes SOD, GSH-Px and plasma levels of MDA were significantly increased but melatonin content of the blood was significantly decreased as compared to nonsmokers. In spite of an increase in antioxidant enzyme activities, MDA levels were slightly increased in smokers. This indicates that antioxidant self-defence mechanisms may not sufficiently protect the respiratory system from smoke-mediated oxidative injury. This result may be related to low melatonin levels in teenage female smokers. It seems that melatonin can reduce free radical damage to the respiratory system induced by cigarette smoke. Further experimental investigations with exogenous melatonin treatments will be needed.

No effects of 900 MHz and 1800 MHz electromagnetic field emitted from cellular phone on nocturnal serum melatonin levels in rats.

In this study, the effects of exposure to a 900 MHz and 1800 MHz electromagnetic field (EMF) on serum nocturnal melatonin levels of adult male Sprague-Dawley rats were studied. Thirty rats were used in three independent groups, 10 of which were exposed to 900 MHz, 10 of which were exposed to 1800 MHz and 10 of which were sham-exposed (control). The exposures were performed 30 min/day, for five days/week for four weeks to 900 MHz or 1800 MHz EMF Control animals were kept under the same environmental conditions as the study groups except with no EMF exposure. The concentration of nocturnal melatonin in the rat serum was measured by using a radioimmunoassay method. There were no statistically significant differences in serum melatonin concentrations between the 900 MHz EMF group and the sham-exposed group (P > 0.05). The values at 12:00 pm were 39.11 +/- 6.5 pg/mL in the sham-exposed group and 34.97 +/- 5.1 pg/mL in the 900 MHz EMF-exposed group. Also, there were no statistically significant differences in serum melatonin concentrations between the sham-exposed group and the 1800 MHz EMF-exposed group (P > 0.05). The values at 12:00 pm were 39.11 +/- 6.5 pg/mL in the sham-exposed group and 37.96 +/- 7.4 pg/mL in the exposed group. These results indicate that mobile phones, emitting 900 and 1800 MHz EMF, have no effect on nocturnal serum melatonin levels in rats.

Effects of 900 MHz electromagnetic field on TSH and thyroid hormones in rats.

In this study, the effects of exposure to a 900 megahertz (MHz) electromagnetic field (EMF) on serum thyroid stimulating hormone (TSH) and triiodothronine-thyroxin (T3-T4) hormones levels of adult male Sprague-Dawley rats were studied. Thirty rats were used in three independent groups, 10 of which were control (without stress and EMF), 10 of which were exposed to 900 MHz EMF and 10 of which were sham-exposed. The exposures were performed 30 min/day, for 5 days/week for 4 weeks to 900 MHz EMF. Sham-exposed animals were kept under the same environmental conditions as the study groups except with no EMF exposure. The concentration of TSH and T3-T4 hormones in the rat serum was measured by using an immunoradiometric assay (IRMA) method for TSH and a radio-immunoassay (RIA) method for T3 and T4 hormones. TSH values and T3-T4 at the 900 MHz EMF group were significantly lower than the sham-exposed group (p<0.01). There were no statistically significant differences in serum TSH values and T3-T4 hormone concentrations between the control and the sham-exposed group (p>0.05). These results indicate that 900 MHz EMF emitted by cellular telephones decrease serum TSH and T3-T4 levels.