The effects of prenatal and neonatal exposure to electromagnetic fields on infant rat myocardium

Introduction: Electromagnetic fields (EMF) have adverse effects as a result of widespread use of electromagnetic energy on biological systems. The aim of this study was to investigate the effects of prenatal exposure to EMF on rat myocardium by biochemical and histopathological evaluations

The effects of prenatal and postnatal exposure to electromagnetic field on rat ovarian tissue

Exposure to an electromagnetic field (EMF) can have adverse effects on many organs and tissues, including the reproductive system. This study aimed to investigate the effects of EMF exposure during prenatal and postnatal periods on ovarian development in rat offspring. In this study, rat pups born from eight pregnant rats were used. EMF exposure was initiated on the first day of pregnancy and continued until the 42nd postnatal day. The blood and ovarian tissue samples of female offspring in sham and EMF groups were collected when they reached the age of 42 days. Follicle-stimulating hormone levels were significantly higher in the EMF group than in the sham group. Estradiol levels were significantly lower in the EMF group than in the sham group. Tissue-inducible nitric oxide synthase (iNOS) levels and expression were significantly greater in the EMF group than in the sham group. In the EMF group, congestion, bleeding areas, and degeneration of follicle structures were observed in ovarian tissue. The findings suggest that exposure to 50-Hz, 3-mT EMF used in this study during prenatal and postnatal periods may lead to impaired ovarian structure and function in female offspring. EMF may affect ovarian physiology by increasing iNOS levels and may lead to fertility disorders

The Effects of Prenatal and Postnatal Exposure to 50-Hz and 3 mT Electromagnetic Field on Rat Testicular Development

Background and objectives: It has been shown that electromagnetic fields (EMFs) have negative effects on the reproductive system. The biological effects of EMF on the male reproductive system are controversial and vary depending on the frequency and exposure time. Although a limited number of studies have focused on the structural and functional effects of EMF, the effects of prenatal and postnatal EMF exposure on testes are not clear. We aimed to investigate the effects of 50-Hz, 3-mT EMF exposure (5 days/wk, 4 h/day) during pre- and postnatal periods on testis development. Materials and Methods: Pups from three groups of Sprague-Dawley pregnant rats were used: Sham, EMF-28 (EMF-exposure applied during pregnancy and until postnatal day 28), EMF-42 (EMF-exposure applied during pregnancy and until postnatal day 42). The testis tissues and blood samples of male offspring were collected on the postnatal day 42. Results: Morphometric analyses showed a decrease in seminiferous tubule diameter as a result of testicular degeneration in the EMF-42 group. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were decreased in the EMF-42 group. Lipid peroxidation levels were increased in both EMF groups, while antioxidant levels were decreased only in the EMF-28 group. We found decreased levels of vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF1) in the EMF-42 group, and decreased levels of the SRC homology 3 (SH3) and multiple ankyrin repeat domain (SHANK3) in the EMF-28 group in the testis tissue. Conclusions: EMF exposure during pre- and postnatal periods may cause deterioration in the structure and function of testis and decrease in growing factors that would affect testicular functions in male rat pups. In addition to the oxidative stress observed in testis, decreased SHANK3, VEGF, and IGF1 protein levels suggests that these proteins may be mediators in testis affected by EMF exposure. This study shows that EMF exposure during embryonic development and adolescence can cause apoptosis and structural changes in the testis

The Protective Effects of Fucoidan on Cisplatin Induced Testicular Cytotoxicity in Rats

Cisplatin is prevalently used as a chemotherapeutic agent for testis cancer, ovarian cancer, bladder cancer, brain tumors and many cancers such as those. Infertility and sterility may emerge, after treatment with chemotherapeutic agents, depending on patient characteristics and the dose of chemotherapeutic agent. Fucoidan is a sulfated polysaccharide, which is derived from brown seaweeds. It is first isolated in 1913 from marine brown algae by Henrik Kylin. Fucoidan is especially found in the cell-wall of marine brown algae. Many effects of fucoidan such as anti-inflammatory, anti-viral, anti-complement, anti-cancer, anti-oxidant and anti-coagulant effects have been revealed by many studies in the literature. Furthermore, some studies suggest that fucoidan may enhance the antineoplastic effects of anticancer drugs. Besides beneficial effects of fucoidan, no toxic or adverse effect has been shown to date. In this study, we aimed to investigate the effects of fucoidan on testicular tissue and its effects on cisplatin induced testicular damage when used concomitantly with cisplatin

Antioxidant and antiapoptotic activities of deprenyl and estradiol co-administration in aged rat kidney

Aging is a progressive degeneration process in living organisms. Deprenyl is an irreversible monoamineoxidase B inhibitor which has antioxidant, antiapoptotic and neuroprotective effects. Estradiol is also a neuroprotective and antioxidant hormone. The objective of this study was to determine whether the antioxidative effects of deprenyl can suppress apoptotic activity, with or without estradiol, in aged female rat kidney. Wistar Albino female rats were divided into six groups as follows; young (3 months old) control, aged (24 months old) control, aged deprenyl treated, aged estradiol treated, aged deprenyl plus estradiol treated and sham. All rats except for the sham group were injected for 21 days. Determination of oxidative stress parameter was performed spectrophotometrically. To detect apoptotic cells, TUNEL staining and caspase-3 immunohistochemistry were performed. Deprenyl and estradiol administration, alone or in combination, decreased significantly the levels of lipid peroxidation relative to aged control and sham-injected rats. The number of TUNEL positive cells decreased significantly in deprenyl and estradioltreated rats compared with aged control and sham rats. Deprenyl and estradiol replacement attenuated age-related changes in renal morphology. The results indicate that deprenyl treatment alone, or in combination with estradiol, may modulate age-related apoptotic changes in rat kidney by decreasing oxidative stress

The effects of bee venom on liver and skeletal muscle in exhaustive swimming rats

Oxidative damage and proinflammatory cytokines are involved in exhaustive exercise-induced fatigue. This study aimed to investigate the effects of bee venom, a natural toxin, on fatigue and tissue damage in rats that underwent forced swimming exercise. Rats were divided into four groups: control, swimming exercise (SE), bee venom (BV) and swimming exercise + bee venom (SE + BV). SE and SE + BV groups were subjected to forced swimming (load of 7% body weight) for 5 days. BV and SE + BV groups were injected with 1 mg/kg BV subcutaneously. Swimming time, blood lactate and TNF-α levels, MDA and GSH levels in liver and gastrocnemius muscle were evaluated. Swimming time was shorter in SE + BV group than SE group. There was no difference in lactate levels between SE and SE + BV groups. MDA and GSH levels were increased in SE, BV and SE + BV groups. TNF-α levels were increased in BV group compared to control and SE groups. Our study demonstrated that BV administration before exhaustive exercise in rats did not provide anti-fatigue effect. Additionally, BV did not show anti-inflammatory activity and had different effects on antioxidant capacity at tissue level. Further research might explore the effects of different doses and durations of BV on exhaustive exercise

Carnosine attenuates oxidative stress and apoptosis in transient cerebral ischemia in rats

Cerebral ischemia leads to cognitive decline and neuronal damage in the hippocampus. Reactive oxygen species (ROS) play an important role in the neuronal loss after cerebral ischemia and reperfusion injury. Carnosine has both antioxidant and neuroprotective effects against ROS. In the present study, the effects of carnosine on oxidative stress, apoptotic neuronal cell death and spatial memory following transient cerebral ischemia in rats were investigated. Transient ischemia was induced by occlusion of right common carotid artery of rats for 30 min and reperfusion for 24 h or 1 week. Rats received intraperitoneal injection of 250 mg/kg carnosine or saline 30 min prior to experiment. Determination of antioxidant enzyme activities was performed spectrophotometrically. To detect apoptotic cells, TUNEL staining was performed using an In Situ Cell Death Detection Kit. Carnosine treatment elicited a significant decrease in lipid peroxidation and increase in antioxidant enzyme activities in ischemic rat brains. The number of TUNEL-positive cells was decreased significantly in carnosine-treated group when compared with the ischemia-induction group. Carnosine treatment did not provide significant protection from ischemia induced deficits in spatial learning. The results show that carnosine is effective as a prophylactic treatment for brain tissue when it is administered before ischemia without affecting spatial memory

Experimental research Effect of 1α-25-dihydroxyvitamin D 3 on intimal hyperplasia developing in vascular anastomoses: a rabbit model

INTRODUCTION: A common problem encountered in routine daily practice of cardiovascular surgery is migration of smooth muscle cells leading to intimal hyperplasia developing at vascular anastomosis sites which then causes luminal narrowing. The aim of this study was to investigate the antiproliferative effect of 1,25 (OH)(2)D(3) on intimal hyperplasia. MATERIAL AND METHODS: Twenty-one male white New Zealand rabbits weighing 2-3 kg were selected. There were 3 groups of animals each consisting of 7 rabbits. Group 1 was the control group. Group 2 was the sham group and group 3 consisted of rabbits receiving 1,25 (OH)(2)D(3). The right carotid arteries of the subjects in groups 2 and 3 were transected and re-anastomosed. A daily dose of 25 ng 1,25 (OH)(2)D(3) per 100 g body weight was administered for 14 days to rabbits in group 3. Rabbits in group 2 were not subject to any pharmaceutical agent. All the subjects were sacrificed at the end of the 28(th) postoperative day. Their right carotid arteries were resected and then investigated histopathologically. RESULTS: Intimal thickness and intimal area were measured as significantly lower in group 1 when compared with the other groups (p = 0.004). In group 3, the ratios of thickness of tunica intima/thickness of tunica media and area of tunica intima/area of tunica media were significantly lower than those of group 2 (p = 0.015, p = 0.003). CONCLUSIONS: 1,25 (OH)(2)D(3), the active metabolite of vitamin D, reduces the intimal hyperplasia developing after vascular anastomoses

Potential Novel Biomarkers for Diabetic Testicular Damage in Streptozotocin-Induced Diabetic Rats: Nerve Growth Factor Beta and Vascular Endothelial Growth Factor

Background. It is well known that diabetes mellitus may cause testicular damage. Vascular endothelial growth factor (VEGF) and nerve growth factor beta (NGF-β) are important neurotrophic factors for male reproductive system. Objective. We aimed to investigate the correlation between testicular damage and testicular VEGF and NGF-β levels in diabetic rats. Methods. Diabetes was induced by streptozotocin (STZ, 45 mg/kg/i.p.) in adult rats. Five weeks later testicular tissue was removed; testicular VEGF and NGF-β levels were measured by ELISA. Testicular damage was detected by using hematoxylin and eosin staining and periodic acid-Schiff staining, and apoptosis was identified by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). Seminiferous tubular sperm formation was evaluated using Johnsen’s score. Results. In diabetic rats, seminiferous tubule diameter was found to be decreased; basement membrane was found to be thickened in seminiferous tubules and degenerated germ cells. Additionally, TUNEL-positive cells were increased in number of VEGF+ cells and levels of VEGF and NGF-β were decreased in diabetic testes. Correlation between VEGF and NGF-β levels was strong. Conclusion. These results suggest that the decrease of VEGF and NGF-β levels is associated with the increase of the apoptosis and testicular damage in diabetic rats. Testis VEGF and NGF-β levels could be potential novel biomarkers for diabetes induced testicular damage