The effects of mobile phone exposure on mast cells in rat dura mater / Efectos de la exposición del teléfono móvil en los mastocitos de la duramadre de ratas

Mobile phone use has increased rapidly. The central nervous system has been shown to be adversely affected by its electromagnetic field (EMF) resulting in headache and sleep disturbances. How the cells make up the CNS and are affected by EMF is unclear. However, because of their central role in inflammation through diverse stimuli including radiation, this study aimed to investigate the effects of electromagnetic fields induced by mobile phones on mast cells in rat dura mater. A total of 18 adult, female, SpragueDawley rats were divided into two groups. The choice of female rats for his study was based on recent surveys demonstrating that mobile phone use is more frequent and prolonged among females. The study group was exposed to 900 MHz electromagnetic field (1 h/day for 45 days). In the end of the study, duramater tissue was extracted and stained using Toluidine blue. Mast cells were counted and results were analysed using Student t test. Mean mast cell number was 202.33±9.82 and 456.78±35.01 in the control and study groups, respectively (p<0.05). Analysis of serum electrolyte and immunoglobulin E levels showed no statistically significant difference between the two groups (p>0.05). The study showed that mobile phone exposure increased mast cell number and degranulation in rat dura mater. Further studies are required to evaluate the clinical implications of these findings.

El uso del teléfono móvil ha aumentado rápidamente. Se ha demostrado que el sistema nervioso central (SNC) se ve afectado de manera adversa debido al campo electromagnético (CEM) que produce dolor de cabeza y trastornos del sueño. No está claro cómo se ve afectada la composición celular del SNC por el CEM. Sin embargo, debido a su función principal en la inflamación a través de diversos estímulos que incluyen la radiación, este estudio tuvo como objetivo investigar los efectos de los campos electromagnéticos inducidos por los teléfonos móviles en los mastocitos de la duramadre de ratas. Un total de 18 ratas Sprague-Dawley adultas, hembras, se dividieron en dos grupos. Se usaron ratas hembras para este estudio en base a investigaciones recientes que han demostrado que el uso de teléfonos móviles es más frecuente y prolongado en las mujeres. Los grupos de estudio fueron expuestos a un campo electromagnético de 900 MHz (1 h / día durante 45 días). Al término del estudio, fue extirpado el tejido de la duramadre y teñido con azul de toluidina. Se contaron los mastocitos y se analizaron los resultados utilizando la prueba t de Student. La cantidad media de células cebadas fue de 202,33 ± 9.82 y 456,78 ± 35,01 en los grupos control y estudio, respectivamente (p <0,05). El análisis del electrolito sérico y los niveles de inmunoglobulina E no mostraron diferencias estadísticamente significativas entre los dos grupos (p> 0,05). El estudio mostró que la exposición a teléfonos móviles aumentó el número de mastocitos y la desgranulación en la duramadre de las ratas. Se requieren estudios adicionales para evaluar las implicaciones clínicas de estos hallazgos.

The protective effects of whortleberry extract against cisplatin-induced ototoxicity in rats.

INTRODUCTION: Cisplatin is one of the main chemotherapeutic agents used for the treatment of many types of cancer. However, ototoxicity, one of the most serious side effects of cisplatin, restricts its usage. OBJECTIVE: We aimed to investigate the protective effects of whortleberry extract against cisplatin-induced ototoxicity by evaluating hearing and histopathological cochlear damage and by measuring the biochemical parameters affected byoxidative stress. METHODS: Forty-eight male rats were included in the study after performing Distortion Product Otoacoustic Emission test to confirm that their hearing levels were normal. The rats were randomly divided into six groups: the control group, the sham group, and, which received only whortleberry extract, only cisplatin, cisplatin+100mg whortleberry extract, cisplatin+200mg whortleberry extract, respectively. Audiologic investigation was performed by performing the Distortion Product Otoacoustic Emission test at the beginning and at the eighth day of the study. Cardiac blood samples were collected for biochemical analysis, and the rats were sacrificed to obtain cochlear histopathological specimens on the eighth day. RESULTS: The results revealed that whortleberry protects hearing against cisplatin-induced ototoxicity independent of the dose. However, high doses of whortleberry extract are needed to prevent histopathological degeneration and oxidative stress. CONCLUSION: The results obtained in this study show that whortleberry extract has a protective effect against cisplatin-induced ototoxicity.

Whortleberry protects kidney against the cisplatin-induced nephrotoxicity: an experimental study.

PURPOSE: This study investigated the antioxidant effects of whortleberry against cisplatin-induced nephrotoxicity in rats. MATERIAL AND METHODS: This study included 48 female Sprague-Dawley rats weighing 263.68 ± 8.29 g. The rats were divided into the following six groups, with eight rats in each group: control, ethanol control, whortleberry control, cisplatin control, 16 mg/kg cisplatin +100 mg/kg whortleberry, and 16 mg/kg cisplatin +200 mg/kg whortleberry groups. Biochemical analysis was performed by measuring total oxidant status and total antioxidant status, histopathological analysis was performed by calculating proximal and distal tubule areas (µm2), and immunohistochemical analysis was performed by determining anti-Caspase-3 immunostaining. Differences among the groups were examined using one-way analysis of variance, and p < .05 was considered statistically significant. RESULTS: Cisplatin treatment decreased the total antioxidant status and increased the total oxidant status and Caspase-3 level. Moreover, it resulted in the dilatation, vacuolization and loss of tubular epithelial cells; and glomerular degeneration and edema in the kidney tissues (p < .05). Treatment with 100 and 200 mg whortleberries increased the total antioxidant status; decreased the total oxidant status and Caspase-3 level and ameliorated distal and proximal tubule degeneration, glomerular degeneration and edema in the kidney tissues (p < .05). CONCLUSIONS: Our results indicate that the antioxidant effects of the whortleberry decrease cisplatin-associated nephrotoxicity.

Protective effects of tumor necrosis factor alpha inhibitors on methotrexate-induced pancreatic toxicity.

BACKGROUND: Methotrexate (MTX), a folate antagonist, is commonly used in the treatment of many different types of cancer and inflammatory diseases, including pancreatic cancer, although its side effects on the pancreas have not yet been researched. The mechanism of MTX-induced toxicity is not well known, and it has been reported in high-dose toxicity studies that the pancreas is sensitive to toxic effects. OBJECTIVES: The aim of our study was to determine whether adalimumab (ADA) has a preventive effect on MTX-induced pancreas toxicity in rats. MATERIAL AND METHODS: The rats were equally and randomly divided into 3 groups (Group 1 comprised the healthy controls, Group 2 was the MTX group, and Group 3 was the MTX + ADA group). The rats in Groups 2 and 3 received an intraperitoneal (ip.) single-dose injection of MTX (20 mg/kg). A single dose of 5 mg/kg ADA (REMICADE®) was administered ip. to Group 3. All the rats were sacrificed under anesthesia 5 days after receiving the MTX injection. RESULTS: Significantly higher mean edema, necrotic cell, and inflammatory scores were recorded in Groups 2 and 3 compared to those recorded in Group 1. Significantly decreased edema, number of necrotic cells, and inflammatory scores were noted in Group 3 than in Group 2. A decrease in islets of Langerhans cell insulin and somatostatin-positive interneurons was demonstrated after the administration of MTX. An increase in insulin and somatostatin-positive cells in islets of Langerhans, as well as a remodeling of the structure of the pancreas, was shown following treatment with ADA. CONCLUSIONS: Adalimumab was demonstrated to have a protective effect against MTX-induced pancreatic injury in this study.

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats.

BACKGROUND: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. MATERIALS AND METHODS: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. RESULTS: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. CONCLUSIONS: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

Sciatic nerve injury following analgesic drug injection in rats: A histopathological examination.

OBJECTIVE: Sciatic nerve neuropathy can be observed following intramuscular gluteal injections. The histopathological examination of sciatic nerve damage following intramuscular injection in the gluteal region for acute pain treatment is not feasible in humans due to the inability to dissect and examine the nerve tissue. To overcome this issue, we used a rat model for demonstrating damage to the sciatic nerve tissue after the application of commonly used drug injections. METHODS: We investigated possible damage following the intramuscular injection of diclofenac, lornoxicam, morphine, and pethidine in a rat model based on histopathological characteristics such as myelin degeneration, axon degeneration, epineurium degeneration, fibrosis, epineurium thickening, perineurium thickening, lymphocyte infiltration, vacuolization, and edema. RESULTS: All the analgesic drugs used in our study induced histopathological changes in the sciatic nerve. Anti-S100 positivity, showing nerve damage, was found to be the lowest in the group treated with diclofenac. Neurotoxic effects of diclofenac on the sciatic nerve were greater than those of the other drugs used in the study. Lornoxicam induced the least histopathological changes in the nerve. CONCLUSION: Diclofenac induced severe nerve damage not only after direct injection in the sciatic nerve but also after injection in the area around the nerve. Thus, we recommend restricting the use of intramuscular gluteal injections of diclofenac. Intramuscular use of morphine and pethidine should also be overviewed.

The Effects of Curcumin on Wound Healing in a Rat Model of Nasal Mucosal Trauma.

We explored the effects of topical curcumin on the healing of nasal mucosal wounds. A total of 32 Sprague-Dawley Albino rats were randomized in equal numbers into four groups, and unilateral nasal wounds were created using an interdental brush. Group 1 (the sham-control group) contained untreated rats with traumatized right-side nasal cavities; Group 2 and 3 rats were similarly traumatized and treated with topical curcumin (5 and 10 mg/mL) dissolved in dimethyl sulfoxide daily for 7 days after trauma; Group 4 rats were treated with topical dimethyl sulfoxide only. All rats were decapitated on day 15 and the healing sites evaluated by blinded observers in terms of the presence of cellular hyperplasia, goblet cell hypertrophy and degeneration, leucocytic infiltration, ciliary loss and degeneration, edema, and vascular dilation. On histopathological evaluation, all of cellular hyperplasia, leukocytic infiltration, and edema were significantly reduced in Group 3 compared with Group 1 (p = 0.001, p = 0.004, and p = 0.008, resp.). Thus, curcumin reduced the inflammatory response and significantly accelerated wound healing.

Effects of exposure to 2100MHz GSM-like radiofrequency electromagnetic field on auditory system of rats.

INTRODUCTION: The use of mobile phones has become widespread in recent years. Although beneficial from the communication viewpoint, the electromagnetic fields generated by mobile phones may cause unwanted biological changes in the human body. OBJECTIVE: In this study, we aimed to evaluate the effects of 2100MHz Global System for Mobile communication (GSM-like) electromagnetic field, generated by an electromagnetic fields generator, on the auditory system of rats by using electrophysiological, histopathologic and immunohistochemical methods. METHODS: Fourteen adult Wistar albino rats were included in the study. The rats were divided randomly into two groups of seven rats each. The study group was exposed continuously for 30days to a 2100MHz electromagnetic fields with a signal level (power) of 5.4dBm (3.47mW) to simulate the talk mode on a mobile phone. The control group was not exposed to the aforementioned electromagnetic fields. After 30days, the Auditory Brainstem Responses of both groups were recorded and the rats were sacrificed. The cochlear nuclei were evaluated by histopathologic and immunohistochemical methods. RESULTS: The Auditory Brainstem Responses records of the two groups did not differ significantly. The histopathologic analysis showed increased degeneration signs in the study group (p=0.007). In addition, immunohistochemical analysis revealed increased apoptotic index in the study group compared to that in the control group (p=0.002). CONCLUSION: The results support that long-term exposure to a GSM-like 2100MHz electromagnetic fields causes an increase in neuronal degeneration and apoptosis in the auditory system.

Infliximab Modulates Cisplatin-Induced Hepatotoxicity in Rats.

BACKGROUND: Cisplatin (Cis) is one of the most commonly used antineoplastic drugs. It is used as chemotherapy for many solid organ malignancies such as brain, neck, male and female urogenital, vesical and pulmonary cancers. Infliximab blocks tumor necrosis factor alpha (TNF-α). Several studies have reported that infliximab ameliorates cell damage by reducing cytokine levels. AIMS: We aimed to investigate whether infliximab has a preventive effect against cisplatin-induced hepatotoxicity and whether it has a synergistic effect when combined with Cis. STUDY DESIGN: Animal experimentation. METHODS: Male Wistar albino rats were divided in three groups as follows: Cis group, infliximab + Cis (CIN) group and the control group. Each group comprised 10 animals. Animals in the Cis group received an intraperitoneal single-dose injection of Cis (7 mg/kg). In the CIN group, a single dose of infliximab (7 mg/kg) was administered 72 h prior to the Cis injection. After 72 h, a single dose of Cis (7 mg/kg) was administered. All rats were sacrificed five days after Cis injection. RESULTS: TNF-α levels in the Cis group were significantly higher (345.5±40.0 pg/mg protein) than those of the control (278.7±62.1 pg/mg protein, p=0.003) and CIN groups (239.0±64.2 pg/mg protein, p=0.013). The Cis group was found to have high carbonic anhydrase (CA)-II and low carbamoyl phosphate synthetase-1 (CPS-1) levels. Aspartate transaminase (AST) and alanine transaminase (ALT) levels were lower in the CIN group as compared to the Cis group. Total histological damage was greater in the Cis group as compared to the control and CIN groups. CONCLUSION: Cis may lead to liver damage by increasing cytokine levels. It may increase oxidative stress-induced tissue damage by increasing carbonic anhydrase II (CA-II) enzyme levels and decreasing CPS-1 enzyme levels. Infliximab decreases Cis-induced hepatic damage by blocking TNF-α and it may also protect against liver damage by regulating CPS-1 and CA-II enzyme levels.

Histopathological effects of intramuscular metamizole sodium on rat sciatic nerve.

OBJECTIVES: We investigated the histopathological effects of metamizole sodium (MS) on the sciatic nerve. MATERIALS AND METHODS: This study was performed using 48 adult male Wistar albino rats. Ten groups were constituted with 6 rats in each group. MS injection into the sciatic nerve (group 1), MS injection into the muscle [group 3 (50 mg/kg, 0.4 ml) and group 5 (50 mg/kg, 0.8 ml)], MS injection into the muscle cavity in the vicinity of the sciatic nerve [group 2 (50 mg/kg, 0.4 ml) and group 4 (50 mg/kg, 0.8 ml)], normal saline injection into the muscle in the vicinity of the sciatic nerve [group 6A (0.4 ml) and 6B (0.8 ml)], subjected to injury by drilling the entire layer of nerve without injecting any drug, normal saline injection in the sciatic nerve, and control group. Nerve and muscle samples were taken 7 days after administrations. Tissue sections were stained using a hematoxylin and eosin-Luxol® fast blue stain, assessed by a histologist. RESULTS: The levels of axonal degeneration of the rats in groups 1, 2, 3, 4, 5, 6A, and 8 were found to be significantly higher compared to the levels of the rats in the control group (P<0.05). Myelin degeneration of the rats in all groups was found to be significantly higher compared to myelin degeneration of the rats in the control group (P<0.05). CONCLUSION: It was observed that MS could lead to injury in the sciatic nerve with a toxic effect due to diffusion.

The Protective Effect of Adalimumab on Renal Injury in a Model of Abdominal Aorta Cross-Clamping.

BACKGROUND: Adalimumab (ADA) is a potent inhibitor of tumor necrosis factor (TNF-α). ADA treatment suppresses proinflammatory cytokines, leading to a decrease or inhibition of the inflammatory process. OBJECTIVES: The aim of this study was to investigate the possible protective effects of ADA on oxidative stress and cellular damage on rat kidney tissue after ischemia/reperfusion (I/R). MATERIAL AND METHODS: A total of 30 male Wistar albino rats were divided into three groups: control, I/R, and I/R plus ADA (I/R + ADA); each group comprised 10 animals. The control group underwent laparotomy without I/R injury. After undergoing laparotomy, I/R groups underwent two hours of infrarenal abdominal aortic cross ligation, which was followed by two hours of reperfusion. ADA (50 mg/kg) was administered as a single dose, intraperitoneally, to the I/R + ADA group, 5 days before I/R. RESULTS: The I/R group's TNF-α (1150.9 ± 145.6 pg/mg protein), IL-1ß (287.0 ± 32.4 pg/mg protein) and IL-6 (1085.6 ± 56.7 pg/mg protein) levels were significantly higher than those of the control (916.1 ± 88.7 pg/mg protein, p = 0.003; 187.5 ± 37.2 pg/mg protein, p < 0.001; 881.4 ± 57.1 pg/mg protein, p < 0.001, respectively) and I/R + ADA groups (864.2 ± 169.4 pg/mg protein, p = 0.003; 241.4 ± 33.4 pg/mg protein, p = 0.010; 987.7 ± 66.5 pg/mg protein, p = 0.004, respectively). To date, a few histopathological changes have been reported regarding renal I/R injury in rats due to ADA treatment whereas I/R caused severe histopathological injury to kidney tissue. CONCLUSIONS: ADA treatment significantly attenuated the severity of kidney I/R injury, inhibiting I/R-induced oxidative stress and renal damage. Because of its anti-inflammatory and antioxidant effects, ADA pretreatment may have protective effects on experimental kidney injury.

The protective effect of infliximab against carbon tetrachloride-induced acute lung injury.

OBJECTIVES: Carbon tetrachloride (CCl4) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl4 induced lung injury. MATERIALS AND METHODS: Rats were divided into control, CCl4, and CCl4+Ib groups. A single dose of 2 ml/kg CCI4 was administered to CCI4 group and a single dose of 7 mg/kg Ib was given to CCl4+Ib group 24 hr before applying CCI4. RESULTS: TNF-α, malondialdehyde (MDA), nitric oxide (NO) and caspase-3 levels of the CCl4 group were markedly higher than both the control and CCl4+Ib groups. The CCI4+Ib group had lower histopathological injury than the CCl4 group. CONCLUSION: Ib as a strong TNF-α blocker decreases the production of proinflammatory cytokines, MDA, and oxidative stress leading to a protective effect against CCl4 induced lung tissue injury.

The acute effects of preoperative ozone theraphy on surgical wound healing.

PURPOSE: To investigate the effects of preoperative rectal ozone insufflation on surgical wound healing over the proinflammatory cytokines and histopathological changes. METHODS: Twenty one rabbits were divided into 3 groups. Sham, surgical wound, and ozone applied (6 sessions, every other day 70 µg/mL in 12 mL O2-O3 mixture rectally) surgical wound groups were created. TNF-alpha and IL-6 levels from all rabbits were studied at the basal, 24th hour, and 72nd hour. The histopathological examination was done by removing the surgical scar tissue at the end of 72nd hour. RESULTS: TNF-alfa and IL-6 levels were significantly lower compared to the control group, in the rabbits treated with ozone. The increase in angiogenesis, the decrease in the number of inflammatory cells, epidermal and dermal regeneration, better collagen deposition, and increased keratinisation in stratum corneum were observed in the histopathological examination. It was determined that the wound healing noticeably accelerated in the ozone group. CONCLUSION: Preoperative rectal ozone insufflation had a positive effect on surgical wound healing in acute period.

The Effects of Infliximab on Laminin, NFκB, and Anti-TNF Expression through Its Effect on Ischemic Liver Tissue.

The aim of this study was to investigate the possible protective effects of infliximab on expression of laminin, anti-TNF, and NFκB in the rat hepatic cells after ischemia/reperfusion (I/R). A total of 30 male Wistar albino rats were divided into three groups: Control (C), sham I/R (ISC), and I/R+ infliximab (ISC inf); each group comprised 10 animals. C group animals underwent laparotomy without I/R injury. In ISC groups after undergoing laparotomy, 1 hour of superior mesenteric artery ligation was done, which was followed by 1 hour of reperfusion. In the ISC inf group, 3 days before I/R, infliximab (3 mg/kg) was administered intravenously. All animals were killed at the end of reperfusion and hepatic tissue samples were obtained for histopathological and histochemical investigations in all groups. Laminin, anti-TNF, and NFκB immunoreactivity were performed for all groups. ISC caused severe histopathological injury including mucosal erosions, inflammatory cell infiltration, necrosis, hemorrhage, and villous congestion. Infliximab treatment significantly attenuated the severity of intestinal I/R injury and it is shown by laminin, anti-TNF, and NFκB immunoreactivity. Because of its anti-inflammatory and antioxidant effects, infliximab pretreatment may have protective effects on hepatic cells in the experimental intestinal I/R model of rats.

The effect of prenatal exposure to 1800 MHz electromagnetic field on calcineurin and bone development in rats.

PURPOSE: To investigated the effects of exposure to an 1800 MHz electromagnetic field (EMF) on bone development during the prenatal period in rats. METHODS: Pregnant rats in the experimental group were exposed to radiation for six, 12, and 24 hours daily for 20 days. No radiation was given to the pregnant rats in the control group. We distributed the newborn rats into four groups according to prenatal EMF exposure as follows: Group 1 was not exposed to EMF; groups 2, 3, and 4 were exposed to EMF for six, 12, and 24 hours a day, respectively. The rats were evaluated at the end of the 60th day following birth. RESULTS: Increasing the duration of EMF exposure during the prenatal period resulted in a significant reduction of resting cartilage levels and a significant increase in the number of apoptotic chondrocytes and myocytes. There was also a reduction in calcineurin activities in both bone and muscle tissues. We observed that the development of the femur, tibia, and ulna were negatively affected, especially with a daily EMF exposure of 24 hours. CONCLUSION: Bone and muscle tissue development was negatively affected due to prenatal exposure to 1800 MHz radiofrequency electromagnetic field.

The effect of prenatal exposure to 1800 MHz electromagnetic field on calcineurin and bone development in rats

PURPOSE: To investigated the effects of exposure to an 1800 MHz electromagnetic field (EMF) on bone development during the prenatal period in rats. METHODS: Pregnant rats in the experimental group were exposed to radiation for six, 12, and 24 hours daily for 20 days. No radiation was given to the pregnant rats in the control group. We distributed the newborn rats into four groups according to prenatal EMF exposure as follows: Group 1 was not exposed to EMF; groups 2, 3, and 4 were exposed to EMF for six, 12, and 24 hours a day, respectively. The rats were evaluated at the end of the 60th day following birth. RESULTS: Increasing the duration of EMF exposure during the prenatal period resulted in a significant reduction of resting cartilage levels and a significant increase in the number of apoptotic chondrocytes and myocytes. There was also a reduction in calcineurin activities in both bone and muscle tissues. We observed that the development of the femur, tibia, and ulna were negatively affected, especially with a daily EMF exposure of 24 hours. CONCLUSION: Bone and muscle tissue development was negatively affected due to prenatal exposure to 1800 MHz radiofrequency electromagnetic field.

Mobile phone radiation during pubertal development has no effect on testicular histology in rats.

Mobile phones are extensively used throughout the world. There is a growing concern about the possible public health hazards posed by electromagnetic radiation emitted from mobile phones. Potential health risk applies particularly to the most intensive mobile phone users-typically, young people. The aim of this study was to investigate the effects of mobile phone exposure to the testes, by assessing the histopathological and biochemical changes in the testicular germ cells of rats during pubertal development. A total of 12 male Sprague Dawley rats were used. The study group (n = 6) was exposed to a mobile phone for 1 h a day for 45 days, while the control group (n = 6) remained unexposed. The testes were processed with routine paraffin histology and sectioned. They were stained with hematoxylin-eosin, caspase 3, and Ki-67 and then photographed. No changes were observed between the groups (p > 0.05). The interstitial connective tissue and cells of the exposed group were of normal morphology. No abnormalities in the histological appearance of the seminiferous tubules, including the spermatogenic cycle stage, were observed. Our study demonstrated that mobile phones with a low specific absorption rate have no harmful effects on pubertal rat testicles.

Biochemical, Histopathological and Immunohistochemical Evaluation of the Protective and Therapeutic Effects of Thymoquinone against Ischemia and Ischemia/Reperfusion Injury in the Rat Ovary.

AIM: To evaluate the antioxidant effects of thymoquinone (TQ) and to investigate the biochemical, histopathological and immunohistochemical changes in experimental rat ovarian torsion. METHODS: A total of 48 female adult rats were used in this study and randomly divided into 7 groups: (1) sham operation; (2) bilateral 3-hour ovarian ischemia; (3) 3-hour ischemia and 3-hour reperfusion; (4) and (5) rats were administered 20 and 40 mg/kg of TQ, respectively, before 0.5 h of ischemia, and then 3 h of ovarian ischemia was applied; (6) and (7) 3-hour ovarian ischemia was applied; 2.5 h after the induction of ischemia, rats were administered the same doses of TQ; at the end of 3 h of ischemia, a 3-hour reperfusion was applied. Histologic changes under light microscopy, immunoreactivity for anticaspase-3 and serum levels of malondialdehyde, interleukin-6, catalase and glutathione peroxidase were noted and compared between the 7 groups. RESULTS: Ischemia and ischemia/reperfusion cause a deterioration of biochemical and histopathological parameters. Administration of TQ seems to reverse these alterations and alleviate the injury. Antioxidant defense mechanisms appear to be enhanced by the administration of TQ. CONCLUSION: TQ at different doses attenuates ovarian ischemia and ischemia/reperfusion injury in rats.

Biochemical and histopathological effects on the rat testis after exposure to electromagnetic field during fetal period.

OBJECTIVES: Electromagnetic radiation (ER) emitted from cell phones may exert a detrimental influence on human health and may affect the man reproductive system. We aimed to study the biological and morphological effects on the testes of 60-day-old male rats after ER exposure (900 MHz), which was applied continuously throughout embryogenesis. METHODS: A total of six pregnant Sprague Dawley rats were included in the study. Three pregnant rats (experimental group) were exposed to radiation from a cell phone set to talking mode for 24 hours a day for 20 days, and the other 3 pregnant rats (control group) were not to exposed to radiation. Newborn male rats were included from the experimental group (n=7) and the control group (n=7). At the end of 60 days, the rats' testes were excised, and testis length, width, depth, and weight were measured. Histopathological examinations were compared and serum testosterone (T) levels were assayed biochemically. RESULTS: While serum T level (3.51±0.21 ng/ml) of ER Exposed group was significantly lower than the control group (4.04±0.47 ng/ml, p=0.018), Caspase-3 enzyme activity (2.00±0.88) was significantly higher than the control group control (1.00±0.63, p=0.026). Johnsen score (8.4±0.5) of ER group was fairly lower than the control group (9.4±0.5, p=0.010). CONCLUSION: Our study demonstrated that ER exposure throughout embryogenesis may cause reductions in serum total T levels and in the size and weight of the testes of male rats, while causing modest increase in apoptosis.

Protective Effect of Infliximab Against Carbon Tetrachloride-Induced Hepatotoxicity.

Carbon tetrachloride (CCl4), a solvent frequently used in industry, can cause acute liver failure and liver fibrosis. Infliximab (Ib), a potent tumor necrosis factor alpha blocker, has a protective effect on the liver. Therefore, we investigated the protective effect of Ib against CCl4-induced acute liver injury. In this study, 24 male Sprague Dawley rats were randomly divided into three groups: the control group (n = 8), the CCl4 group (n = 8), and the CCl4 + Ib group (n = 8). A single dose of 2 mL/kg CCL4 was administered to the CCL4 group. The CCl4 + Ib group was injected with a single dose (7 mg/kg) of Ib 24 h before CCl4 was administered. In the CCl4 group, the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and the liver tissue levels of transforming growth factor beta 1 (TGF-ß1), interleukin 1 beta (IL-1ß), and adenosine deaminase (ADA) were significantly higher than the levels of these same substances in the control and CCl4 + Ib groups. The histopathological investigation revealed that although there was excessive liver injury in the CCl4 group, there was reduced injury in the CCl4 + Ib group. In addition, the carbamoyl phosphate synthetase I (CPS-I) and carbonic anhydrase II (CA-II) levels in the CCl4 group were significantly lower than those in the control and CCl4 + Ib groups. The results show that during CCl4-induced hepatotoxicity, Ib prevents liver injury by suppressing TGF-ß1 and IL-1ß levels, decreasing ADA levels, and regulating CPS-I and CA-II enzyme levels.