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Background: Electromagnetic fields (EMF) have teratogenic effects during the embryonic development. In current study, histopathological and physiological effects of sinusoidal EMF on the brain were investigated. We sought to determine the apoptosis level and changes in blood brain barrier permeability in brain tissue of pre-incubated white leghorn hen eggs in the field of EMF. Materials and Methods: In this experimental study, 300 healthy, fresh, and fertilized eggs (55-65 g) were divided into experimental (3 groups, N=50), control (N=75) and sham (N=75) groups. Experimental eggs (inside the coil) were exposed to 3 different intensities of 1.33, 2.66 and 7.32 mT and sham groups were also located inside the same coil but with no exposure, for 24 hrs before incubation. Control, sham and experimental groups were incubated in an incubator (38±0.5ºC, 60% humidity). Brains of 14 day old chicken embryos of all groups were removed, fixed in formalin (10%), stained with H & E and TUNEL, apoptotic cells were studied under light microscope. Brains of other embryos were prepared for scanning electron microscope. By injections of Evans blue, any possible changes in brain vessels were also investigated. Results: Our results showed electromagnetic fields have toxic effects on cell organelles and cell membranes. EMF would increase the level of cellular apoptosis in the brain. They also would tear up the blood vessels. Thereafter, they would affect the permeability of blood brain barrier of exposed chicken embryos. Conclusion: These findings suggest that electromagnetic fields induce different degrees of brain damages in chicken embryos brain tissue.

Ischemic tolerance can protect the brain against cerebral ischemia and neurodegenerative diseases. However, several studies demonstrate ischemic tolerance by various methods, the exact mechanisms of ischemic tolerance has not been clearly understood. In this study, we first studied brain ischemia-related mechanisms and then evaluated the outcomes of mitochondrial pathophysiology of ischemic tolerance in focal and full stroke animal models. In this study, mitochondrial and peroxisomal reactions are considered critical in ischemic tolerance. In rats and Syrian mice, the middle cerebral artery occlusion (MCAO) model was employed to represent cerebrovascular stroke. Ischemic tolerance exhibits different types of adaptation responses associated with a number of sub-cellular changes. Changes in the cellular non-genomic pathways are usually short and reversible; while, the consequences of genes expression are a long-term process and can lead to permanent alternations in the genes expression pattern. The ischemic tolerance can be clinically significant. Therefore, it is important to address the risks and advantages of ischemic tolerance in non-infarcted tissues such as transplanted ones.

Background Products of oxidation are known to trigger cancer through damaging cellular components and angiogenesis backs tumor growth and metastasis. Antioxidant enzymes like superoxide dismutase and catalase fight the stress posed by these products. Angiogenesis inhibition offers additional benefits toward tumor suppression. Nigella sativa L. is a plant traditionally used in Middle Eastern countries for its various benefits. Objectives In this study, we attempted to examine the anti-tumor, antioxidant and antiangiogenic effects of N. sativa crude oil in breast tumor-bearing mice. Materials and Methods In this experimental study, three groups of female BALB/c mice, 5 animals in each, were respectively treated for a month with 1, 2 and 4 mL/kg/day of N. sativa oil 2 days after subcutaneous tumor transplantation. The fourth group, the control group, after subcutaneous tumor transplantation received distilled water. Tumor volumes, antioxidant enzymes’ activity, endostatin and vascular endothelial growth factor (VEGF) amounts were measured to study N. sativa crude oil’s proposed effects. Results In comparison with the control group, mice receiving doses of 2 and 4 mL/kg/day of N. sativa crude oil had significantly reduced tumor volumes (P < 0.005), less VEGF (P < 0.005), more endostatin (P < 0.05 and P < 0.005, respectively) and increased superoxide dismutase (SOD) (P < 0.05 and P < 0.005, respectively) and catalase (CAT) activity (P < 0.005). Conclusions N. sativa crude oil seems to inhibit breast tumor growth partly through improving the activity of antioxidant enzymes’ activity and partly by suppressing angiogenesis. Yet, more studies are required to intensely clarify the other involved mechanisms.