The apoptotic effects of bisphenol A exposure on the rat ovary: an experimental study.

Bisphenol A (BPA) is a key endocrine-disrupting chemical (EDC) in the manufacturing industry. It is found in the structure of compounds such as polycarbonate and epoxy in combination with other chemicals. Our objective was to investigate the effect of BPA on rat ovaries. A total of 32 female rats were divided into four equal groups: In group 1 (control), vehicle was administered; in group 2, BPA 50 µg/day was administered intraperitoneally; in group 3, BPA 100 mg/kg/day was administered intraperitoneally; and in group 4, BPA 100 mg/kg/day and vitamin C (50 mg/kg) were administered intraperitoneally, while vitamin E (50 mg/kg) was administered intramuscularly. Thirty days after the treatment, the effects of BPA on the ovaries were evaluated by terminal deoxynucleotidyltransferase [TdT]-mediated dUTP-biotin nick end labeling (TUNEL) assay. There was no difference in the number of apoptotic cells between group 2 and group 4. In addition, there was no significant difference between control group and group 2, 4. However, the number of apoptotic cells per unit area was significantly increased in group 3 compared with all groups (p < 0.01, p < 0.05). In conclusion, this study showed that high doses of BPA (100 mg/kg/day) have a toxic effect on the ovaries. The fact that the number of apoptotic cells in the group administered with high dose of BPA + 50 mg/kg/day vitamin C + 50 mg/kg/day vitamin E was lower than that of the high-dose BPA-administered group shows that these vitamins may have a protective effect.

Effects of Quercetin on Lipid and Protein Damage in the Liver of Streptozotocin-Induced Experimental Diabetic Rats.

Quercetin (QR) is part of a subclass of flavonoids called flavonols. We aimed to investigate the effect of QR on malondialdehyde (MDA), advanced oxidation protein products (AOPPs), and glutathione peroxidase (GSH-Px) activity in the liver of diabetic rats. We compared four groups of male adult Wistar albino rats: a control group, an untreated diabetic group, diabetic groups treated with QR, and QR group. Diabetes was induced by a single injection of streptozotocin (STZ) (50 mg/kg). Animals were kept in standard condition. On the 31st day of the study, the liver tissue was removed for biochemical parameters and histopathological evaluations. In an untreated diabetic group, liver MDA and AOPP levels were significantly higher than all groups. QR treatment significantly decreased the increased MDA, AOPP levels, and increased the decreased GSH-Px enzyme activity in liver tissues. The QR-treated rats in the diabetic group showed an improved histological appearance. Lesser vesicular vacuolization and fibrotic areas were observed in the QR-treated diabetic group than in the diabetic group. The STZ-induced liver injury is associated with oxidative stress, and coadministration of QR may reduce this damage effectively in a rat model. Our results are also supported by morphological improvement in liver tissue. Therefore, we think QR may be effective in treating hyperglycemia and oxidative damage in diabetes.

Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells.

There is a widespread use of 2.4 GHz electromagnetic radiation emitting devices especially in communication and education. Recent studies show the adverse effects of electromagnetic fields (EMF) such as oxidative stress, cellular damage and apoptosis on tissues. Selenium (Se) has an antioxidant properties by inhibiting oxidative damage being within the structure of antioxidant enzymes like glutathione peroxidase (GSH-Px) and it has also regulatory function for cell cycle and apoptosis. The aim of this study was to investigate the effect of Se on 2.4 GHz frequency EMF exposed human embryonic kidney cells (HEK293) by means of alterations in apoptotic and oxidative stress parameters. Our study was planned as control, EMF, 100 nM Se + EMF, 200 nM Se + EMF groups. EMF groups were exposed to 2.4 GHz EMF for 1 h, element groups were incubated with two different doses of Se added cell culture medium for 48 h before EMF exposure. MDA levels were significantly higher whereas SOD and GSH-Px activities were significantly lower in EMF compared to control. 100 and 200 nM Se + EMF application decreased MDA levels, increased SOD and GSH-Px activities than EMF. Apoptosis and caspase-3 were statistically significantly higher but bcl-2 was lower in EMF than control. Apoptosis and caspase-3 were lower in 100 and 200 nM Se + EMF, although bcl-2 were higher than EMF. In conclusion, Se has protective effects against 2.4 GHz EMF-induced oxidative stress by reducing lipid peroxidation, regulating SOD and GSH-Px activity. Also, Se has inhibitory effect on 2.4 GHz EMF induced apoptosis by increasing the expression of anti-apoptotic protein bcl-2 and suppressing apoptosis regulatory protein caspase-3.

Hemostasis vs. epidural fibrosis?: A comparative study on an experimental rat model of laminectomy.

AIM: The aim of this study was to evaluate the histopathological and biochemical impact and effectiveness of two hemostatic agents, Ankaferd blood stopper (ABS) and Microporous Polysaccharide Hemospheres (MPH), on epidural fibrosis in an experimental rat laminectomy model. MATERIAL AND METHODS: Twenty adult Wistar albino rats were divided into MPH-treated (n=6), ABS-treated (n=6) and control (n=8) groups. Laminectomy of the lumbar spine was performed in all animals and treatment groups were exposed to MPH and ABS while closure was applied in control group as per usual. Epidural fibrosis was evaluated in all groups macroscopically, histopathologically, biochemically and with electron microscopy four weeks later. RESULTS: Statistically, it was found that MPH-treated group had significantly less epidural fibrosis compared to ABS-treated and control groups. CONCLUSION: We compared two hemostatic agents for their propensity to cause adhesions in the present study. Our results show that MPH significantly reduces epidural scar formation and dural adhesion in a rat model of laminectomy while ABS increases postoperative fibrosis.

Protective effect of melatonin and 1,25-dihydroxyvitamin D3 on renal ischemia-reperfusion injury in rats.

Ischemia-reperfusion (I/R) injury induces the generation of reactive oxygen species (ROS) which affect many organs. This study was designed to investigate the roles of melatonin and 1,25-dihydroxyvitamin D3 (VD3) on renal I/R injury. Thirty male Wistar albino rats were divided into five groups: group 1, control; group 2, right nephrectomy (RN) +  I/R in the contralateral kidney; group 3, melatonin + RN + I/R; group 4, VD3 + RN + I/R; and group 5, melatonin + VD3 + RN + I/R. Melatonin (10 mg/kg), VD3 (0.5 µg/kg), and melatonin plus VD3 were injected intraperitoneally for 7 days before renal I/R. After 7 days, right nephrectomy was initially performed and left renal artery was clamped for 45 min. After 45-min reperfusion, the serum and kidney tissue samples were obtained for assays. Melatonin and VD3 had an ameliorative effect on biochemical parameters such as serum creatinine (SCr) and blood urea nitrogen (BUN). Renal tissue malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels, and superoxide dismutase (SOD) activity were determined. Renal I/R decreased the kidney tissue GSH levels and SOD activity and increased the NO levels as compared with control group. However, melatonin and VD3 and melatonin plus VD3 treatment significantly increased the tissue GSH levels and SOD activity and decreased the NO levels compared with those of I/R group. Meanwhile, MDA levels were not different between the control and I/R groups. But, MDA levels decreased in all treated groups compared to I/R and control groups. These data support that melatonin and VD3 have beneficial effects on renal injury.

AR-A014418 as a glycogen synthase kinase-3 inhibitor: anti-apoptotic and therapeutic potential in experimental spinal cord injury.

OBJECTIVES: We aimed to investigate the effects of AR-A014418, a strong inhibitor specific to GSK-3beta, on neuronal apoptosis and neuroprotection in the traumatic SCI model. MATERIALS AND METHODS: In this study, three groups were generated from 36 Wistar rats; (1) control, (2) spinal cord trauma group created by clip compression technique after laminectomy, and (3) AR-A014418 (4mg/kg, i.p., DMSO) treatment group after laminectomy and spinal cord trauma. The TUNEL assay for apoptosis detection, immunohistochemical staining for bax and TGF-beta were applied in spinal cord tissues. For light microscopic examination, necrotic, and apoptotic cells were counted, and PMNL counting was applied to detect inflammation. Functional recovery was tested by field locomotor test in the 3rd and 7th days following surgery. RESULTS: In the trauma group, diffuse hemorrhage, cavitation, necrosis and edematous regions, degeneration in motor neurons and leukocyte infiltration were observed in gray matter. In the AR-A014418-treated groups, healthy cells were observed in more places compared to the trauma groups, however, cavitation, hemorrhagic, and edematous areas were seen in gray matter. In the AR-A014418-treatment groups, the number of apoptotic cells in the 3rd and 7th days (respectively; p<0.05, p<0.01), were significantly decreased compared to the trauma groups, as were the levels of bax (p<0.01) and TGF-beta 1 immunoreactivity. Results of the locomotor test were significantly increased in the treatment group (p<0.001) as compared to the trauma group. CONCLUSIONS: In this experimental spinal cord trauma model study neural apoptosis was significantly triggered in secondary damage developed after trauma, however, neurological healing was expedited by preventing mitochondrial apoptosis and reducing the inflammation by the potent inhibitor AR-A014418, which is GSK-3beta selective.

Zinc supplementation attenuates metallothionein and oxidative stress changes in kidney of streptozotocin-induced diabetic rats.

Zinc is an element that under physiological conditions preferentially binds to and is a potent inducer of metallothionein under physiological conditions. The present study was conducted to explore whether zinc supplementation morphologically and biochemically protects against diabetic nephropathy through modulation of kidney metallothionein induction and oxidative stress in streptozotocin-induced diabetic rats. Thirty-two Wistar albino male rats were equally divided into four groups. The first group was used as untreated controls and the second group was supplemented with 30 mg/kg/day zinc as zinc sulfate. The third group was treated with streptozotocin to induce diabetes and the fourth group was treated with streptozotocin and supplemented with zinc as described for group 2. The blood glucose and micro-albuminuria levels, body and kidney weights were measured during the 42-day experimental period. At the end of the experiment, the kidneys were removed from all animals from the four groups. Diabetes resulted in degenerative kidney morphological changes. The metallothionein immunoreactivity level was lower and the kidney lipid peroxidation levels were higher in the diabetes group than in the controls. The metallothionein immunoreactivity levels were higher in the tubules of the zinc-supplemented diabetic rats as compared to the non-supplemented diabetic group. The zinc and metallothionein concentrations in kidney tissue were higher in the supplemented diabetic group compared to the non-supplemented diabetes group. The activity of glutathione peroxidase did not change in any of the four groups. In conclusion, the present study shows that zinc has a protective effect against diabetic damage of kidney tissue through stimulation of metallothionein synthesis and regulation of the oxidative stress.