Does Radiofrequency Radiation From Mobile Phones Affect the Formation of Parotid Gland Malignancy? An Experimental Study.

Objectives: The use of mobile phone is increasing around the world. Although it is beneficial in terms of communication, the electromagnetic radiations emitted by mobile phones may cause undesirable biological effects on the human body. In practical use, the tissue with which mobile phones come into most and are closest is the parotid gland. This study investigated the effects of the 1800 MHz electromagnetic field created by a generator on the parotid gland in rats. Methods: A total of 21 Sprague-Dawley Albino rats were included in the study. The rats were randomly divided into three equal groups. To simulate a mobile phone in conversation mode, the first study group was exposed to an 1800-MHz electromagnetic field for 6 hours a day for 30 days, and the second study group was exposed to an 1800-MHz electromagnetic field for 12 hours a day for 30 days. After 30 days, rats were sacrificed, and histopathological and immunohistochemical methods were used to evaluate the effects on the parotid gland. The total antioxidant level and the total oxidant level were measured biochemically in homogenized parotid tissue. Results: Histopathological results showed an increase in degeneration in rats exposed to electromagnetic fields for 6 and 12 hours a day, and immunohistochemical analysis showed an increase in the apoptotic index in both study groups (P = .001, P < .001). Intranuclear inclusions was observed during histopathological examination performed by electron microscopy. Conclusions: This study observed that the 1800 MHz electromagnetic field caused undesirable adverse histopathological and biochemical effects on the parotid gland of rats. Histopathological and biochemical findings were detected with increasing contact and exposure time. This study will lead to other studies on this topic and contribute to the literature by completing other studies.

Comparative Analysis of Epigallocatechin-3-Gallate and TNF-Alpha Inhibitors in Mitigating Cisplatin-Induced Pancreatic Damage Through Oxidative Stress and Apoptosis Pathways.

Oxidative stress and inflammation caused by cisplatin, which is frequently used in the treatment of many cancers, damage healthy tissues as well as cancer cells. In this study, we aimed to investigate the effect of epigallocatechin-3-gallate (EGCG) and infliximab (INF) administration on pancreatic endocrine cells in rats treated with systemic cisplatin (CDDP). The rats were randomly divided into 6 groups: group 1 (control group), group 2 (EGCG group), group 3 (CDDP group), group 4 (EGCG + CDDP group), group 5 (CDDP + INF group), and group 6 (EGCG + CDDP + INF group). The study's findings demonstrated that EGCG and INF effectively reduced the cellular damage induced by CDDP in histopathologic investigations of the pancreas. EGCG and INF, whether used individually or in combination, demonstrated a significant reduction in malondialdehyde (MDA) levels and an increase in glutathione (GSH) levels in the rat pancreas compared to the CDDP group. Immunohistochemically, the enhanced presence of insulin and glucagon positivity in the EGCG and INF groups, along with the absence of TUNEL immunopositivity, indicate that both treatments reduced CDDP-induced apoptosis. Furthermore, the observed lack of immunopositivity in TNF-α and 8-OHdG in the groups treated with EGCG and INF, compared to those treated with CDDP, indicates that these substances can inhibit inflammation. EGCG and INF, whether provided alone or together, can potentially reduce the damage caused to pancreatic islet cells by cisplatin. This effect is achieved through their anti-inflammatory and antioxidant properties during the early stages of the condition.

Preventive effects of melatonin on periodontal tissue destruction due to psychological stress in rats with experimentally induced periodontitis.

OBJECTIVE AND BACKGROUND: Psychological stress is a potential modifiable environmental risk factor causally related to the exacerbation of periodontitis and other chronic inflammatory diseases. This animal study aimed to investigate comprehensively the preventive efficacy of systemic melatonin administration on the possible effects of restraint stress on the periodontal structures of rats with periodontitis. METHODS: Forty-eight male Sprague Dawley rats were randomly divided into six groups: control, restraint stress (S), S-melatonin (S-Mel), experimental periodontitis (Ep), S-Ep, and S-Ep-Mel. Periodontitis was induced by placing a 3.0 silk suture in a sub-paramarginal position around the cervix of the right and left lower first molars of the rats and keeping the suture in place for 5 weeks. Restraint stress was applied simultaneously by ligation. Melatonin and carriers were administered to the control, S, Ep, and S-Ep groups intraperitoneally (10 mg/body weight/day, 14 days) starting on day 21 following ligation and subjection to restraint stress. An open field test was performed on all groups on day 35 of the study. Periodontal bone loss was measured via histological sections. Histomorphometric and immunohistochemical (RANKL and OPG) evaluations were performed on right mandibular tissue samples and biochemical (TOS (total oxidant status), TAS (total antioxidant status), OSI (oxidative stress index), IL-1ß, IL-10, and IL-1ß/IL-10) evaluations were performed on left mandibular tissue samples. RESULTS: Melatonin significantly limited serum corticosterone elevation related to restraint stress (p < .05). Restraint stress aggravated alveolar bone loss in rats with periodontitis, while systemic melatonin administration significantly reduced stress-related periodontal bone loss. According to the biochemical analyses, melatonin significantly lowered IL-1ß/IL-10, OSI (TOS/TAS), and RANKL/OPG rates, which were significantly elevated in the S-Ep group. CONCLUSION: Melatonin can significantly prevent the limited destructive effects of stress on periodontal tissues by suppressing RANKL-related osteoclastogenesis and oxidative stress.

The potential antioxidant effect of N-acetylcysteine on X-ray ionizing radiation-induced pancreas islet cell toxicity.

PURPOSE: Previous research has highlighted the impact of X-ray irradiation-induced organ damage, on cancer patients after radiation therapy. The ionizing radiation-induced oxidative stress causes injury to the pancreatic islet cells of Langerhans. We used histopathological, immunohistochemical, and biochemical analyses to examine α- and ß-cells in the islets of Langerhans in rats undergoing whole-body x-ray ionizing radiation, a group of which was treated with NAC. MATERIAL AND METHODS: Twenty-four male rats were randomly divided into 3 groups, one control, and two experimental groups. Group I (Control) was administered only saline solution (0.09% NaCl) by oral gavage for 7 days. Group II (IR) was administrated whole body single dose 6 Gray ionizing radiation (IR) and saline solution (0.09% NaCl) by oral gavage for 7 days. Group III (IR + NAC) was administered 300 mg/kg NAC (N-acetylcysteine) by oral gavage for 7 days, 5 days before, and 2 days after 6 Gray IR application. RESULTS: In the X-ray irradiation group, we observed diffuse necrotic endocrine cells in the islets of Langerhans. In addition, we found that Caspase-3, malondialdehyde (MDA) levels increased, and insulin, glucagon, and glutathione (GSH) levels decreased in the IR group compared to the control group. In contrast, we observed a decrease in Caspase-3, and MDA levels in necrotic endocrine cells, and an increase in insulin, glucagon, and GSH levels in the IR + NAC group compared to the IR group. CONCLUSION: This study provides evidence for the beneficial effects of N-acetyl cysteine on islets of Langerhans cells with X-ray ionizing-radiation-induced damage in a rat model.

Resveratrol Attenuates Degeneration and Apoptosis of Cardiomyocytes Induced by Aortic Clamping.

INTRODUCTION: Objective: To investigate the potential beneficial effects of resveratrol (RVT) against ischemia-reperfusion injury of myocardial tissue during surgical treatment of ruptured abdominal aortic aneurysm. METHODS: Four groups were established - control, ischemia/reperfusion (I/R), sham (I/R+solvent/dimethyl sulfoxide [DMSO]), and I/R+RVT. Ruptured abdominal aortic aneurysm model was used as the experimental protocol. RESULTS: In the I/R and I/R+DMSO groups, malondialdehyde (MDA) levels in myocardial tissue were found to be significantly increased compared to the control group. The MDA level in myocardial tissue was significantly decreased in the I/ R+RVT group compared to the I/R group. In I/R and I/R+DMSO groups, glutathione peroxidase (GSH) levels in myocardial tissue were found to be significantly decreased compared to the control group. The GSH level in the myocardial tissue was significantly increased in the I/R+RVT group compared to the I/R group. In the light microscope, isotropic and anisotropic band disorganized atypical cardiomyocytes in the I/R group and degenerative cardiomyocytes and edematous areas in the I/R+DMSO group were observed. Degenerative cardiomyocytes and edematous areas were decreased in the I/R+RVT group. When heart tissue sections incubated with cleaved caspase-3 primary antibodies were examined under the light microscope, apoptotic cardiomyocytes were present in I/R and I/R+DMSO groups. A decrease in the number of apoptotic cardiomyocytes was observed in the I/R+RVT group. CONCLUSION: The findings of the present study indicate that RVT exhibits protective effects against ischemia-reperfusion injury occurring in the myocardium as a distant organ as a result of abdominal aorta clamping.

Protective Effect of Vaccinium myrtillus Extract on X-ray Irradiation-Induced Retinal Toxicity via eNOS and 8-OHdGexpression.

Every year, hundreds of thousands of cancer patients receive radiotherapy treatment. Oxidative stress is observed in healthy tissues due to irradiation exposure. The present study is the first to address the effects of Vaccinium myrtillus (whortleberry, WB) against the effects of x-ray irradiation on retinal tissue. Twenty-four Sprague-Dawley rats were randomly allocated into 4 groups: (1) control group: rats without any treatment, (2) x-ray irradiation group: 8 Gray (Gy) RT for 2 days, (3) 100 mg WB extract + x-ray irradiation group: 8 Gy irradiation for 2 days and followed by intraperitoneal (IP) WB extract (100 mg/kg) supplementation for 10 days, (4) 200 mg WB extract + x-ray irradiation group: 8 Gy irradiation for 2 days and followed by intraperitoneal (IP) WB extract (200 mg/kg) supplementation for 10 days. Eyes were enucleated on the 10th day after RT for histopathological, immunohistochemical (8-hydroxy deoxyguanosine (8-OHdG), endothelial nitric oxide synthase (eNOS), and biochemical analyses (glutathione peroxidase (GSH), and malondialdehyde (MDA). The GSH levels significantly decreased and MDA levels and 8-OHdG staining increased after x-ray irradiation compared to the control group. Combined x-ray irradiation +WB treatment significantly increased GSH levels and significantly decreased MDA production and 8-OHdG staining. However, eNOS staining was not affected in any of the groups. Besides, x-ray irradiation significantly increased cell losses and edematous areas. The WB significantly reversed the cellular damage in ganglion cells, inner nuclear, and outer nuclear layers in quantitative analyses. The x-ray irradiation caused significant retinal impairment, and additional WB therapy provided protective effects against radiation-induced retinopathy. These results may suggest WB extract as an adjuvant therapy to reverse retinal impairments after x-ray irradiation.

Agomelatine on cisplatin-induced nephrotoxicity via oxidative stress and apoptosis.

Drug-induced nephrotoxicity is the greatest deterrent to the use of cisplatin, which is a frequently used chemotherapeutic with proven effectiveness in cancer therapy. Agomelatine, which is used in the treatment of sleep disorders and depression, has gained attention in recent years with its antioxidative and anti-inflammatory effects. In this study, the effects of the synthetic melatonin agonist agomelatine on nephrotoxicity were investigated in a rat model of cisplatin-induced nephrotoxicity using biochemical, histological, and immunohistochemical methods. Thirty-two male rats were divided into 4 groups: 1. control group, 2. agomelatine group, 3. cisplatin group, 4. cisplatin + agomelatine group. In the cisplatin group, there were widespread atypical glomerular structures and vacuolization in tubular epithelial cells, necrotic tubules, deterioration of brush border structure in proximal tubules, and fibrotic areas characterized by diffuse polymorphonuclear leukocyte (PNL) and extensive collagen deposition in the interstitial spaces. However, in the cisplatin + agomelatine group, we observed a reduction in glomeruli of atypical structure and necrotic tubules, in PNL infiltration in interstitial spaces, and fibrotic areas compared to the cisplatin group. The cisplatin + agomelatine group showed lower malondialdehyde (MDA) serum creatinine, serum urea levels, and higher glutathione (GSH) levels compared to the cisplatin group. Immunohistochemical analyses revealed that the elevated NF-kß/p65, 8-OHdG, and cleaved caspase-3 positivity in the cisplatin group had significantly decreased in the cisplatin + agomelatine group. In conclusion, agomelatine showed a nephroprotective effect against cisplatin-induced nephrotoxicity.

The Effects of Dexmedetomidine on Abdominal Aortic Occlusion-Induced Ovarian Injury via Oxidative Stress and Apoptosis.

Ischemia/reperfusion (I/R) induced ovarian damage is caused by various diseases such as ovarian torsion, ovarian transplantation, cardiovascular surgery, sepsis, or intra-abdominal surgery. I/R-related oxidative damage can impair ovarian functions, from oocyte maturation to fertilization. This study investigated the effects of dexmedetomidine (DEX), which has been shown to exhibit antiapoptotic, anti-inflammatory, and antioxidant effects, on ovarian I/R injury. We designed four study groups: group 1 (n = 6): control group; group 2 (n = 6): only DEX group; group 3 (n = 6): I/R group; group 4 (n = 6): I/R + DEX group. Then, ovarian samples were taken and examined histologically and immunohistochemically, and tissue malondialdehyde (MDA) and glutathione (GSH) levels were measured. In the I/R group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, and follicular degeneration, edema, and inflammation were increased compared to the control group (p = 0.000). In addition, GSH levels were significantly decreased in the I/R group compared to the control group (p = 0.000). On the other hand, in the I/R + DEX treatment group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, follicular degeneration, edema, and inflammation findings were decreased than in the I/R group (p = 0.000, p = 0.005, p = 0.005, p = 0.001, p = 0.005, respectively). However, GSH levels increased significantly in the I/R + DEX treatment group compared to the I/R group (p = 0.000). DEX protects against ovarian I/R injury through antioxidation and by suppressing inflammation and apoptosis.

Resveratrol Attenuates Degeneration and Apoptosis of Cardiomyocytes Induced by Aortic Clamping

ABSTRACT Introduction: Objective: To investigate the potential beneficial effects of resveratrol (RVT) against ischemia-reperfusion injury of myocardial tissue during surgical treatment of ruptured abdominal aortic aneurysm. Methods: Four groups were established — control, ischemia/reperfusion (I/R), sham (I/R+solvent/dimethyl sulfoxide [DMSO]), and I/R+RVT. Ruptured abdominal aortic aneurysm model was used as the experimental protocol. Results: In the I/R and I/R+DMSO groups, malondialdehyde (MDA) levels in myocardial tissue were found to be significantly increased compared to the control group. The MDA level in myocardial tissue was significantly decreased in the I/ R+RVT group compared to the I/R group. In I/R and I/R+DMSO groups, glutathione peroxidase (GSH) levels in myocardial tissue were found to be significantly decreased compared to the control group. The GSH level in the myocardial tissue was significantly increased in the I/R+RVT group compared to the I/R group. In the light microscope, isotropic and anisotropic band disorganized atypical cardiomyocytes in the I/R group and degenerative cardiomyocytes and edematous areas in the I/R+DMSO group were observed. Degenerative cardiomyocytes and edematous areas were decreased in the I/R+RVT group. When heart tissue sections incubated with cleaved caspase-3 primary antibodies were examined under the light microscope, apoptotic cardiomyocytes were present in I/R and I/R+DMSO groups. A decrease in the number of apoptotic cardiomyocytes was observed in the I/R+RVT group. Conclusion: The findings of the present study indicate that RVT exhibits protective effects against ischemia-reperfusion injury occurring in the myocardium as a distant organ as a result of abdominal aorta clamping.

The protective effects of red ginseng and amifostine against renal damage caused by ionizing radiation.

This study aimed to elucidate the effects of amifostine (ethyol) (AM), a synthetic radioprotector, and red ginseng (RG), a natural radioprotective agent, against the toxic effect of ionizing radiation (IR) on kidney tissues through changes in biochemical and histopathological parameters in addition to contributions to the use of amifostine and RG in clinical studies. Five groups were established: Group I (control, receiving only saline by gavage), Group II (IR only), and Group III (IR+AM, 200 mg/kg intraperitoneally (i.p.). Group IV (IR + RG, 200 mg/kg orally once a day for 4 weeks), and Group V (IR+RG+AM, 200 mg/kg orally once/day for 4 weeks before IR and 200 mg/kg AM administered (i.p.) 30 min before IR). All groups, except for the control group, were subject to 6-Gy whole-body IR in a single fraction. 24 h after irradiation, all animals were sacrificed under anesthesia. IR enhanced MDA, 8-OHdG, and caspase-3 expression while decreasing renal tissue GSH levels (p < .05). Significant numbers of necrotic tubules together with diffuse vacuolization in proximal and distal tubule epithelial cells were also observed. The examination also revealed substantial brush boundary loss in proximal tubules as well as relatively unusual glomerular structures. While GSH levels significantly increased in the AM, RG, and AM+RG groups, a decrease in KHDS, MDA, 8-OHdG, and caspase-3 expression was observed, compared to the group subject to IR only (p < .05). Therefore, reactive oxygen species-scavenging antioxidants may represent a promising treatment for avoiding kidney damage in patients receiving radiation.

Dexmedetomidine attenuates pneumocyte apoptosis and inflammation induced by aortic ischemia-reperfusion injury.

OBJECTIVE: Despite significant improvements in interventional vascular aneurysm repair procedures and intensive care patient management, there has been no significant decrease in mortality due to ruptured abdominal aortic aneurysm. Oxidative stress is known to play a key role in secondary organ damage due to infrarenal aortic clamping. The aim of this study was to examine the potential protective effect of the alpha-2 adrenergic receptor agonist dexmedetomidine (DMT) on aortic occlusion-induced lung injury. METHODS: Thirty Sprague Dawley rats were allocated into control, ischemia-reperfusion (IR), and IR+DMT groups randomly. Vascular clamps were attached to the abdominal aorta in the IR and IR+DMT groups. Two-hour reperfusion was established 1 h after ischemia. The IR+DMT group received a single intraperitoneal 100 µg dose of DMT 30 min before infrarenal abdominal aortic clamping. RESULTS: IR due to aortic occlusion led to apoptosis, widespread inflammation, alveolar septal wall thickening due to bleeding and vascular congestion were observed in both types I and II pneumocytes. Malondialdehyde levels increased while glutathione decreased. However, DMT was found to lower apoptotic pneumocytes, alveolar-septal thickness, hemorrhage, vascular congestion, and malondialdehyde levels, while glutathione levels in lung tissue increased. CONCLUSIONS: This study is the first to address the effects of DMT on the lung in a ruptured abdominal aortic aneurysm model. Our findings suggest that the alpha-2 adrenergic receptor agonist DMT reduces oxidative stress and apoptosis, thus protecting against aortic occlusion-induced pulmonary injury.

Effects of gadodiamide and gadoteric acid on lung tissue: A comparative study.

We set out to investigate the effects of gadodiamide and gadoteric acid, used for magnetic resonance imaging, on the lungs. In this study, 32 male Sprague Dawley rats were used. These were allocated into four groups; The first group (control) was untreated. The second group received isotonic saline on the first and fourth days of the week for 5 weeks. Following the same schedule, the third and fourth groups received a total of 2 mg/kg gadodiamide and gadoteric acid, respectively, in place of saline. The alveolar Wall thickness was evaluated. Gadodiamide and gadoteric acid significantly increased the numbers of collagen-3 and caspase-3 positive cells in the lung tissue (p < 0.05). In addition, these two substances increased the alveolar Wall thickness (p < 0.05). Furthermore, they increased the levels of malondialdehyde and glutathione (p < 0.05). This study demonstrates that both linear and macrocyclic contrast agents are toxic for the lungs in rats.

Comparison of effects of dexmedetomidine and amifostine against X-ray radiation-induced parotid damage.

Radiotherapy can be employed as a therapeutic modality alone in the early stages of cancer and is used together with other treatments such as surgery and chemotherapy in more advanced stages. However, exposure to ionizing radiation in association with radiotherapy affects several organs in the head and neck and can give rise to early and late side effects. Exposure to ionizing radiation used in radiotherapy is known to cause cell damage by leading to oxygen stress through the production of free oxygen radicals (such as superoxide radicals, hydroxyl radical, hydrogen peroxide, and singlet oxygen), depending on the total radiation dosage, the fractionation rate, radiosensitivity, and linear energy transfer. The purpose of the present study was to determine the potential protective role of a powerful and highly selective α2-adrenoreceptor agonist with a broad pharmacological spectrum against salivary gland damage induced by ionizing radiation exposure. Forty Sprague-Dawley rats were divided into five groups-control, ionizing radiation, ionizing radiation + dexmedetomidine (100 µg/kg), ionizing radiation + dexmedetomidine (200 µg/kg), and ionizing radiation + amifostine (200 mg/kg). Following exposure to ionizing radiation, we observed necrosis, fibrosis, and vascular congestions in parotid gland epithelial cells. We also observed increases in malondialdehyde (MDA) and cleaved Caspase-3 levels and a decrease in glutathione (GSH). In groups receiving dexmedetomidine, we observed necrotic epithelial cells, fibrosis and vascular congestion in parotid gland tissue, a decrease in MDA levels, and an increase in GSH. Dexmedetomidine may be a promising antioxidant agent for the prevention of oxidative damage following radiation exposure.

Bee pollen increases hippocampal brain-derived neurotrophic factor and suppresses neuroinflammation in adult rats with chronic immobilization stress.

Chronic stress is a potential problem associated with anxiety, depression, and cognitive dysfunction. Bee pollen, a powerful antioxidant, has many therapeutic effects. In this study, we aimed to examine the effects of one of the Anatolian bee pollens on depression/anxiety. 24 male Sprague Dawley rats were divided into 3 groups as control, stress, and bee pollen + stress. Bee pollen (200 mg/kg/day) was given to rats exposed to physical stress for 10 days. Open field test (OFT) and forced swimming test (FST) were applied to monitor the behavioral changes of the rats. After behavioral tests, the rats were euthanized. Brain-derived neurotrophic factor (BDNF), interleukin 1 beta (IL-1ß), and tumor necrosis factor-alpha (TNF-α) levels were measured by ELISA to evaluate neurological and biochemical changes in rat hippocampal tissue. In addition, malondialdehyde (MDA) and glutathione (GSH) levels in the brain were evaluated. According to the behavioral test results, bee pollen reduced anxiety-like behavior but did not affect depression-like behavior. We also found that bee pollen suppressed neuroinflammation while reducing oxidative stress and lipid peroxidation in hippocampal tissues. Moreover, bee pollen significantly increased the level of BDNF in the hippocampus. In conclusion, bee pollen reduced oxidative damage and neuroinflammation caused by immobilization stress in rat brain tissue. Therefore, we suggest that bee pollen may be an effective natural compound in alleviating the negative effects caused by immobilization stress.

Resveratrol against lung injury in an ischemia/reperfusion model of abdominal aortic rupture.

BACKGROUND: The aim of this study was to examine the effects on the lungs of ischemia/reperfusion injury in a ruptured abdominal aortic aneurysm model in rats and to investigate the potential protective effects of resveratrol. METHODS: Thirty-two male Sprague-Dawley rats were randomly divided into four groups: control, ischemia/reperfusion, sham (ischemia/ reperfusion + solvent/dimethyl sulfoxide), and ischemia/reperfusion + resveratrol. In the groups subjected to ischemia/reperfusion, following 60-min shock to the abdominal aorta, vascular clamps were attached from the levels of the infrarenal and iliac bifurcation. A total of 60-min ischemia was applied, followed by 120-min reperfusion. In the ischemia/ reperfusion + resveratrol group, intraperitoneal 10 mg/kg resveratrol was administered 15 min before ischemia and immediately after reperfusion. Malondialdehyde, glutathione, and catalase levels were analyzed and histopathological examination of the lung tissues was performed. RESULTS: Malondialdehyde levels increased in the ischemia/reperfusion and ischemia/reperfusion + dimethyl sulfoxide groups, compared to the control group, while catalase levels decreased, and no significant difference was observed in the glutathione levels. Malondialdehyde levels decreased with the administration of resveratrol, while glutathione levels increased, and catalase levels remained unchanged. The increased inflammation in interstitial spaces, thickening in the alveolar septal walls, increased numbers of cleaved caspase-3 apoptotic pneumocytes, and increased histopathological lung damage scores observed in the ischemia/reperfusion and ischemia/reperfusion + dimethyl sulfoxide groups improved with the application of resveratrol. CONCLUSION: These findings suggest that resveratrol may exhibit a protective effect in preventing acute lung injury developing due to ischemia/reperfusion in ruptured abdominal aortic aneurysm surgery by reducing oxidative damage.

Periodontitis exacerbates the renal degenerative effects of obesity in rats.

BACKGROUND/OBJECTIVES: Obesity and periodontitis are systemic subclinical inflammatory diseases with established negative renal effects. The aim of this animal study was to thoroughly investigate the possible effects of these two diseases on renal structure and function. METHODS: Thirty-two male Sprague Dawley rats were divided into four groups: control (C), obesity (Ob), experimental periodontitis (Ep), and Ob + Ep. The first 16 weeks of the experiment were aimed for the induction of obesity and the last 5 weeks for the induction of periodontitis. Throughout the experimental period, the C and Ep groups were fed standard rat chow, while the Ob groups (Ob and Ob + Ep) were fed high-fat rat chow. Right after the establishment of obesity, periodontal tissue destruction was achieved by placing 3.0 silk sutures in sub-paramarginal position around the cervices of mandibular right-left first molar teeth and preserving them for 5 weeks. On the last day of the 22nd week, following blood collection, all rats were euthanized, and kidneys and mandibles were collected. Alveolar bone loss was measured on microcomputed tomographic slices. Histopathological evaluations (light microscopy, semi-quantitative analysis of renal corpuscle area, and immunohistochemical analysis of caspase-3 activity) were done on right kidneys and biochemical evaluations (malonyl-aldehyde [MDA], glutathione [GSH], total oxidant status [TOS], total antioxidant status [TAS], oxidative stress [OSI], tumor necrosis factor-α [TNF-α], interleukin-1ß [IL-1ß], matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D [CtD] levels) were done on left kidneys. Renal functional status was evaluated with levels of serum creatinine, urea, and cystatin C. RESULTS: Periodontal bone loss was significantly higher in the Ep and Ob + Ep groups, compared with the C and Ob groups (p < .05). All parameters except TAS and GSH were highest in the Ob + Ep group, and the differences were statistically significant compared with the control group (p < .05). Although the mean TAS and GSH levels were lower in the Ob + Ep group than the other groups, the differences were not statistically significant (p > .05). While the atypical glomeruli score was significantly higher in the Ob + Ep group than in all other groups (p < .05), the acute tubular necrosis and histopathological scores were significantly different only compared with the control group (p < .05). CONCLUSION: This experimental study showed that the negative effects of the co-existence of periodontitis and obesity on inflammatory stress and apoptotic changes in the kidneys together with the functional parameters were significantly more severe, compared with the presence of one of these diseases alone. TNF-α could have a central role in the periodontitis and obesity-related structural and functional renal changes.

The hepatoprotective potential of resveratrol in an experimental model of ruptured abdominal aortic aneurysm via oxidative stress and apoptosis.

The mortality rate in ruptured abdominal aortic aneurysms can today be reduced through cardiovascular surgery. However, ischemia and reperfusion-induced tissue damage develop due to aortic cross-clamping applied during surgery. The present study aimed to reduce oxidative stress-induced hepatic damage resulting from ischemia and reperfusion due to aortic cross-clamping during surgery by means of resveratrol administration. Forty male Sprague-Dawley rats were randomly assigned into four groups: control (healthy), glycerol+ischemia/reperfusion (I/R) (sham), I/R, and I/R + Resveratrol. In all groups scheduled for I/R, 60 min of shock was followed by 60 min of ischemia. In the I/R + Resveratrol group, 10 mg/kg of resveratrol was administered 15 min before ischemia and immediately before reperfusion via the intraperitoneal route. In addition, 120 min of reperfusion was applied under anesthesia after ischemia in all groups. Intralobar and interlobar necrosis, vascular congestion, and edematous fields resulting from aortic occlusion were present. Liver tissue malondialdehyde (MDA) levels and cleaved caspase-3 positivity increased, while glutathione (GSH) levels decreased. However, resveratrol administration reduced intralobular and interlobar necrosis, vascular congestion and edematous fields, cleaved caspase-3 positivity, and MDA levels, and increased GSH levels. Our findings suggest that resveratrol is effective against aortic occlusion-induced liver injury by reducing oxidative stress and apoptosis.

Can Dexmedetomidine Be Effective in the Protection of Radiotherapy-Induced Brain Damage in the Rat?

Approximately 7 million people are reported to be undergoing radiotherapy (RT) at any one time in the world. However, it is still not possible to prevent damage to secondary organs that are off-target. This study, therefore, investigated the potential adverse effects of RT on the brain, using cognitive, histopathological, and biochemical methods, and the counteractive effect of the α2-adrenergic receptor agonist dexmedetomidine. Thirty-two male Sprague Dawley rats aged 5-6 months were randomly allocated into four groups: untreated control, and RT, RT + dexmedetomidine-100, and RT + dexmedetomidine-200-treated groups. The passive avoidance test was applied to all groups. The RT groups received total body X-ray irradiation as a single dose of 8 Gy. The rats were sacrificed 24 h after X-ray irradiation, and following the application of the passive avoidance test. The brain tissues were subjected to histological and biochemical evaluation. No statistically significant difference was found between the control and RT groups in terms of passive avoidance outcomes and 8-hydroxy-2'- deoxyguanosine (8-OHdG) positivity. In contrast, a significant increase in tissue MDA and GSH levels and positivity for TUNEL, TNF-α, and nNOS was observed between the control and the irradiation groups (p < 0.05). A significant decrease in these values was observed in the groups receiving dexmedetomidine. Compared with the control group, gradual elevation was determined in GSH levels in the RT group, followed by the RT + dexmedetomidine-100 and RT + dexmedetomidine-200 groups. Dexmedetomidine may be beneficial in countering the adverse effects of RT in the cerebral and hippocampal regions.

Apelin-13 activates the hippocampal BDNF/TrkB signaling pathway and suppresses neuroinflammation in male rats with cisplatin-induced cognitive dysfunction.

It has been established that cisplatin causes neuronal damage and cognitive impairment. However, the mechanism is not sufficiently clear. Apelin-13 is an endogenous peptide with strong neuroprotective effects through the synthesis of neurotrophic factors and suppression of inflammation. The aim of this study was to investigate the role of brain-derived neurotrophic factor/tropomyosin receptor kinase B (BDNF/TrkB) signaling pathway and the potential inhibitory effects of apelin-13 in the mechanism of cisplatin-induced hippocampal damage and cognitive impairment. Apelin-13 was administered to adult sprague dawley male rats at a dose of 20 nmol/kg every day for 4 weeks, cisplatin was administered at a dose of 5 mg/kg once a week for 4 weeks. The spatial and recognition memory tests of the rats were performed on the 5th week. BDNF and the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) levels were measured by ELISA in hippocampal homogenates. Pyramidal neuron and glial cell damage in the hippocampal CA1, CA3 and dentate gyrus (DG) were analyzed histologically. TrkB activity in the hippocampus was determined by immunohistochemical methods. Cisplatin impaired spatial and recognition memory in rats, while apelin-13 improved spatial memory but did not affect recognition memory. Cisplatin suppressed BDNF in the hippocampus while increased IL-1ß and TNF-α. In contrast, apelin-13 administration increased BDNF but significantly suppressed TNF-α and IL-1B. Cisplatin caused pyramidal neuron and glial cell damage in CA1, CA3 and DG. In the cisplatin + apelin-13 group, however, pyramidal neuron and glial cell damage was less than those without apelin-13. Cisplatin increased TrkB activity in the hippocampus, which was counteracted by apelin-13. In conclusion, apelin-13 reduced the cisplatin-induced cognitive deficiency, by suppressing inflammation and stimulating the synthesis and activation of neurotrophic factors in hippocampal tissue.

The protective effect of astaxanthin on cisplatin-induced ototoxicity.

BACKGROUND: Promising studies have been conducted with many substances to reduce the ototoxic effects of cisplatin, but there is no treatment that completely eliminates the ototoxic effect. OBJECTIVES: To determine the effectiveness of astaxanthin (ASX) as a protective agent against cisplatin-induced ototoxicity. MATERIAL AND METHODS: Thirty-six rats were randomly divided into 6 groups. Group 1 received no drug injections except for anesthetics; group 2 received intraperitoneal (IP) olive oil only for 8 days; group 3 received only IP ASX 75 mg/kg dissolved in olive oil for 8 days; group 4 received a single dose of only IP 16 mg/kg cisplatin on the 5th day; group 5 received 25 mg/kg ASX IP daily for 8 days and a single 16 mg/kg dose of cisplatin on the 5th day; group 6 received 75 mg/kg ASX IP daily for 8 days and a single 16 mg/kg dose of cisplatin on the 5th day. The animals were tested for distortion product otoacoustic emissions (DPOAE) before and 3 days after cisplatin treatment. The animals in all groups were sacrificed under anesthesia on the 10th day. Before sacrifice, inferior vena cava blood samples were drawn into commercial tubes for biochemical analysis and their cochlea were prepared for histological analysis. RESULTS: The ASX+cisplatin groups demonstrated significantly higher DPOAE thresholds when compared to the cisplatin-only group (p < 0.05). The ASX 25 mg/kg/day+cisplatin group showed a significant increase in total antioxidant capacity compared to the cisplatin-only group, whereas the ASX 75 mg/kg/day+cisplatin group had significantly lower total oxidative stress and oxidative stress index. Histologic results showed that the cortical organ was better preserved in the ASX+cisplatin groups compared to the cisplatin-only group, and the degeneration in the spiral ganglion and inner and outer hair cells was less visible in the ASX groups. CONCLUSIONS: Astaxanthin can protect hearing from cisplatin-induced ototoxicity, prevent cellular degeneration and significantly reduce oxidative stress.