Tolga Mercantepe

Pathological effects of prenatal exposure to a 900 MHz electromagnetic field on the 21-day-old male rat kidney

Abstract We investigated the effects on kidney tissue of 900 megahertz (MHz) EMF applied during the prenatal period. Pregnant rats were exposed to 900 MHz EMF, 1 h/day, on days 13–21 of pregnancy; no procedure was performed on control group pregnant rats or on mothers or newborns after birth. On postnatal day 21, kidney tissues of male rat pups from both groups were examined by light and electron microscopy. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione levels also were investigated. Light microscopy revealed some degenerative changes in the tubule epithelium, small cystic formations in the primitive tubules and large cysts in the cortico-medullary or medullary regions in the experimental group. Electron microscopy revealed a loss of peritubular capillaries and atypical parietal layer epithelial cells in the experimental group. Biochemical analysis showed significantly increased MDA levels in the experimental group and decreased SOD and CAT levels. EMF applied during the prenatal period can caused pathological changes in kidney tissue in 21-day-old male rats owing to oxidative stress and decreased antioxidant enzyme levels.

The effects of prenatal exposure to a 900-MHz electromagnetic field on the 21-day-old male rat heart

Abstract The growing spread of mobile phone use is raising concerns about the effect on human health of the electromagnetic field (EMF) these devices emit. The purpose of this study was to investigate the effects on rat pup heart tissue of prenatal exposure to a 900 megahertz (MHz) EMF. For this purpose, pregnant rats were divided into experimental and control groups. Experimental group rats were exposed to a 900 MHz EMF (1 h/d) on days 13–21 of pregnancy. Measurements were performed with rats inside the exposure box in order to determine the distribution of EMF intensity. Our measurements showed that pregnant experimental group rats were exposed to a mean electrical field intensity of 13.77 V/m inside the box (0.50 W/m2). This study continued with male rat pups obtained from both groups. Pups were sacrificed on postnatal day 21, and the heart tissues were extracted. Malondialdehyde, superoxide dismutase and catalase values were significantly higher in the experimental group rats, while glutathione values were lower. Light microscopy revealed irregularities in heart muscle fibers and apoptotic changes in the experimental group. Electron microscopy revealed crista loss and swelling in the mitochondria, degeneration in myofibrils and structural impairments in Z bands. Our study results suggest that exposure to EMF in the prenatal period causes oxidative stress and histopathological changes in male rat pup heart tissue.

Can prenatal exposure to a 900 MHz electromagnetic field affect the morphology of the spleen and thymus, and alter biomarkers of oxidative damage in 21-day-old male rats?

We investigated the effects of a 900 Megahertz (MHz) electromagnetic field (EMF), applied during the prenatal period, on the spleen and thymus of 21-day-old male rat pups. Pregnant Sprague-Dawley rats were divided into control and EMF groups. We applied 900 MHz EMF for 1 h/day to the EMF group of pregnant rats. Newborn male rat pups were removed from their mothers and sacrificed on postnatal day 21. Spleen and thymus tissues were excised and examined. Compared to the control group, thymus tissue malondialdehyde levels were significantly higher in the group exposed to EMF, while glutathione levels were significantly decreased. Increased malondialdehyde and glutathione levels were observed in splenic tissue of rats exposed to EMF, while a significant decrease occurred in superoxide dismutase values compared to controls. Transmission electron microscopy showed pathological changes in cell morphology in the thymic and splenic tissues of newborn rats exposed to EMF. Exposure to 900 MHz EMF during the prenatal period can cause pathological and biochemical changes that may compromise the development of the male rat thymus and spleen.

Renoprotective effect of aliskiren on renal ischemia/reperfusion injury in rats: electron microscopy and molecular study

Abstract Purpose: To determine the protective effect of aliskiren on ischemia–reperfusion (I/R) injury in a rat renal (I/R) model. Methods: Rats were randomly divided into five groups: sham control group; sham control with aliskiren pretreatment; I/R group and I/R with two doses of aliskiren pretreatment. Rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 24 h reperfusion. Aliskiren (50 and 100 mg/kg) was administered orally by gavage 24 and 1 h prior to ischemia. After 24 h reperfusion, kidney samples were taken for the determination of malondialdehyde (MDA) level, superoxide dismutase (SOD), glutathione (GSH) activity and histological evaluation. The level of serum creatinine (SCR) and blood urea nitrogen (BUN), renin and angiotensin II (AT-2) was measured in serum samples. Results: Kidneys from I/R groups showed significant increase in MDA level and significant decrease in GSH, and SOD activity. IL-1β, iNOS and NFkB gene expression significantly increased in the I/R groups in the rat kidney tissue. Aliskiren treatment showed a significant down-regulatory effect on IL-1β, iNOS and NFkB mRNA expression. Compared with the sham group, SCR and BUN, renin and AT-2 were significantly increased in the I/R rats, accompanied by histopathological damage to the kidney. Conclusion: Pretreatment with aliskiren ameliorated I/R-induced renal injury through decreasing nitric oxide and AT-2 levels and by the reduction of injury induced by I/R injury and ameliorated renal histopathological molecular and biochemical changes.

Morphological and antioxidant impairments in the spinal cord of male offspring rats following exposure to a continuous 900MHz electromagnetic field during early and mid-adolescence.

The effects of devices emitting electromagnetic field (EMF) on human health have become the subject of intense research among scientists due to the rapid increase in their use. Children and adolescents are particularly attracted to the use of devices emitting EMF, such as mobile phones. The aim of this study was therefore to investigate changes in the spinal cords of male rat pups exposed to the effect of 900MHz EMF. The study began with 24 Sprague-Dawley male rats aged 3 weeks. Three groups containing equal numbers of rats were established-control group (CG), sham group (SG) and EMF group (EMFG). EMFG rats were placed inside an EMF cage every day between postnatal days (PD) 21 and 46 and exposed to the effect of 900MHz EMF for 1h. SG rats were kept in the EMF cage for 1h without being exposed to the effect of EMF. At the end of the study, the spinal cords in the upper thoracic region of all rats were removed. Tissues were collected for biochemistry, light microscopy (LM) and transmission electron microscopic (TEM) examination. Biochemistry results revealed significantly increased malondialdehyde and glutathione levels in EMFG compared to CG and SG, while SG and EMFG catalase and superoxide dismutase levels were significantly higher than those in CG. In EMFG, LM revealed atrophy in the spinal cord, vacuolization, myelin thickening and irregularities in the perikarya. TEM revealed marked loss of myelin sheath integrity and invagination into the axon and broad vacuoles in axoplasm. The study results show that biochemical alterations and pathological changes may occur in the spinal cords of male rats following exposure to 900MHz EMF for 1h a day on PD 21-46.

Protective effects of estrogen and bortezomib in kidney tissue of post-menopausal rats: an ultrastructural study

Abstract Purpose: Symptoms and disorders related to menopause and its associated estrogen deficiency have become a considerable health concern worldwide. Ovarian hormone depletion/estrogen deficiency can be usefully studied using animal models after removal of the ovaries [ovariectomy (Ovx)]. This study assessed renal changes after Ovx-induced estrogen deficiency in a rat model. Methods: Rats were randomly allotted into one control group (group I, healthy) and three study groups (group II, Ovx group; group III, Ovx +17β-estradiol group; and group IV, Ovx + bortezomib group). Results: In the Ovx group (group II), thickening of glomerular capillary walls, narrowing of Bowman’s capsular space, glomerular hypertrophy, atrophic tubules, and loss of the basal membranes of the tubules were observed. Mesangial cell proliferation was observed, particularly in the glomerulus. Immunohistochemical (IHC) staining studies in this group showed dense staining in the mesangial cells, tubular cell Nf-KB/p65, and caspase-3. Groups III and IV (Ovx +17β-estradiol and Ovx + bortezomib) showed decreased NF-kB/p65 and caspase-3 expression compared with the Ovx group (p < 0.05). Conclusion: In renal failure related to estrogen deficiency caused by Ovx, 17β-estradiol and bortezomib have a protective effect on renal tissue.

The Role of RAAS Inhibition by Aliskiren on Paracetamol-Induced Hepatotoxicity Model in Rats.

Paracetamol is one of the most popular and widely used analgesic and antipyretic agents, but an overdose can cause hepatotoxicity and lead to acute liver failure. Aliskiren directly inhibits renin which downregulates the renin–angiotensin–aldosterone system (RAAS). Recent findings suggest that RAAS system takes part in the pathogenesis of liver fibrosis. We aimed to reveal the relationship between hepatotoxicity and the RAAS by examining paracetamol induced hepatotoxicity. Rats were separated into five groups as follows: control, 100 mg/kg aliskiren (p.o.), 2 g/kg paracetamol (per os (p.o.)), 2 g/kg paracetamol + 50mg/kg aliskiren (p.o.), and 2 g/kg paracetamol + 100 mg/kg aliskiren(p.o.). Samples were analyzed at the biochemical, molecular, and histopathological levels. Paracetamol toxicity increased alanine aminotransferases (ALT), aspartate aminotransferases (AST), renin, and angiotensin II levels in the serum samples. In addition, the SOD activity and glutathione (GSH) levels decreased while Lipid Peroxidation (MDA) levels increased in the livers of the rats treated with paracetamol. Paracetamol toxicity caused a significant increase in TNF‐α and TGF‐β. Both aliskiren doses showed an improvement in ALT, AST, oxidative parameters, angiotensin II, and inflammatory cytokines. Only renin levels increased in aliskiren treatment groups due to its pharmacological effect. A histopathological examination of the liver showed that aliskiren administration ameliorated the paracetamol‐induced liver damage. In immunohistochemical staining, the expression of TNF‐α in the cytoplasm of the hepatocytes was increased in the paracetamol group but not in other treatment groups when compared to the control group. In light of these observations, we suggest that the therapeutic administration of aliskiren prevented oxidative stress and cytokine changes and also protected liver tissues during paracetamol toxicity by inhibiting the RAAS. J. Cell. Biochem. 117: 638–646, 2016.

Biochemical and pathological changes in the male rat kidney and bladder following exposure to continuous 900-MHz electromagnetic field on postnatal days 22–59*

Abstract Purpose: To investigate the effect on male rat kidney and bladder tissues of exposure to 900-megahertz (MHz) electromagnetic field (EMF) applied on postnatal days 22–59, inclusive. Materials and methods: Twenty-four male Sprague Dawley rats, aged 21 days, were used. These were divided equally into one of three groups, control (CG), sham (SG) or EMF (EMFG). CG was not exposed to any procedure. SG rats were kept inside a cage, without being exposed to the effect of EMF, for 1 h a day on postnatal days 22–59, inclusive. EMFG rats were exposed to continuous 900-MHz EMF for 1 h a day under the same conditions as those for the SG rats. Rats were sacrificed on postnatal day 60, and the kidney and bladder tissues were removed. Tissues were stained with hematoxylin and eosin (H&E) and Masson trichrome for histomorphological evaluation. The TUNEL method was used to assess apoptosis. Transmission electron microscopy (TEM) was also used for the kidney tissue. Oxidant/antioxidant parameters were studied in terms of biochemical values. Results: The findings showed that tissue malondialdehyde increased in EMFG compared to CG and SG in both kidney (p = 0.004 and p = 0.004, respectively) and bladder tissue (p = 0.004, p = 0.006, respectively), while catalase and glutathione levels decreased compared to CG (p = 0.004; p = 0.004, respectively) and SG (p = 0.004; p = 0.004, respectively). In the EMF group, pathologies such as dilatation and vacuolization in the distal and proximal tubules, degeneration in glomeruli and an increase in cells tending to apoptosis were observed in kidney tissue. In bladder tissue, degeneration in the transitional epithelium and stromal irregularity and an increase in cells tending to apoptosis were observed in EMFG. Additionally, EMFG samples exhibited glomerular capillary degeneration with capillary basement membranes under TEM. Conclusions: We conclude that continuous exposure to the effect of 900-MHz EMF for 1 h a day on postnatal days 22–59, inclusive, causes an increase in oxidative stress and various pathological changes in male rat kidney and bladder tissues.

L-carnitine alleviates sciatic nerve crush injury in rats: functional and electron microscopy assessments.

Several studies have demonstrated that L-carnitine exhibits neuroprotective effects on injured sciatic nerve of rats with diabetes mellitus. It is hypothesized that L-carnitine exhibits neuroprotective effects on injured sciatic nerve of rats. Rat sciatic nerve was crush injured by a forceps and exhibited degenerative changes. After intragastric administration of 50 and 100 mg/kg L-carnitine for 30 days, axon area, myelin sheath area, axon diameter, myelin sheath diameter, and numerical density of the myelinated axons of injured sciatic nerve were similar to normal, and the function of injured sciatic nerve also improved significantly. These findings suggest that L-carnitine exhibits neuroprotective effects on sciatic nerve crush injury in rats.

Protective effects of alpha-lipoic acid on experimental sciatic nerve crush injury in rats: assessed with functional, molecular and electromicroscopic analyses

Aim: The present study aimed to demonstrate protective effects of alpha lipoic acid on experimental sciatic nerve crush injury model assessed with functional and electronmicroscopy analyses. Methods: In this study, groups were; Group 1; sham operated, Group 2; applied only sciatic nerve crush (Control), Group 3; Sciatic nerve crush + treated ALA 25 mg/kg (received orally) and Group 4; Sciatic nerve crush + treated ALA 50 mg/kg. Subsequently, sciatic nerves crush injury induced by forceps. At the second and fourth week, all animals were evaluated for sciatic functional index (SFI) and histomorphometric analyses with electronmicroscopy. Results: The SFI was significantly increased for both ALA-treated groups 30 days post-injury compared with control groups. The elecronmicroscopy results demonstrated that the axon diameter, the myelin diameter, the area of regenerating axon and miyelin were better in the treatment group than in the control group. Also ALA decreased IL-1β and Caspase 3 levels that increased in SNC group. Conclusions: These results suggest that ALA neuroprotective agent for peripheral nerve injury (PNI) and promoted peripheral nerve regeneration via its anti-inflammatory and antiapoptotic effects.