Technological devices such as mobile phones, wi-fi and bluetooth applications used widely in daily life emit low-dose electromagnetic fields (EMFs). EMFs influence metabolic processes in the body and exert various harmful biological effects on cells. This study aims to evaluate acute and chronic effects of 900 MHz EMF exposure on the microscopic structure of rat liver. Twenty-four adult Wistar albino rats were randomly divided into sham-control (Group I), acutely EMF-exposed (Group II) and chronically EMF-exposed (Group III) groups (n = 8 in each). The Rats of Group II were exposed to 900 MHz EMF using a microwave test transmitter during 24 h continuously just for one day. Group III-rats were exposed to 900 MHz EMF for 60 minutes a day for 30 days. Sham-controls were not applied EMF. After the rats were sacrificed under the anesthesia, their livers were removed and processed for light microscopic evaluation. Liver sections stained with histochemical dyes (H&E, PAS and Masson’s trichrome) displayed many histopathological alterations in both of the EMF-exposed groups, including foci of necrosis, inflammation, excessive vacuolar degenerations and apoptosis in hepatocytes, apparent vascular expansions and haemorrhage. Additionally, mononuclear cell infiltrations, biliary hyperplasia, fibrosis in periportal and centrilobular areas and decreased Kupffer cell population were determined in the chronic EMF exposure group. In contrast, the amount of the Kupffer cells were much more in the acute exposure group. Our findings suggested that both acute and chronic exposure to 900 MHz EMFs can lead to hepatic injury in rats.

Testicular torsion mainly affects children and adolescents, and the ischemia/reperfusion (I/R) injury that follows surgical detorsion can impair later fertility. Melatonin studies in this setting have used histological, hormonal, and semen endpoints, which cannot show whether the spermatozoa can still fertilize oocytes and support embryo development. Forty-eight male Wistar rats were assigned to sham, sustained ischemia (I), and I/R (720° torsion for 90 min, then detorsion) groups, each with or without a single intraperitoneal dose of melatonin (10 mg/kg; n = 8/group). After 20 days, testes were evaluated by Johnsen scoring and caspase-3 immunohistochemistry, serum testosterone was measured, and epididymal spermatozoa were analyzed and used for in vitro fertilization (IVF) of pooled oocytes from superovulated females. Both injuries lowered Johnsen scores, testosterone, and sperm concentration, motility, and normal morphology and increased caspase-3 immunoreactivity, with sustained ischemia causing greater damage. Fertilization fell from 55.0% in sham animals to 10.0% (I) and 15.0% (I/R), and blastocyst yield from 35.0% of inseminated oocytes to 2.5% and 7.5%, respectively. Melatonin improved all parameters, increasing fertilization to 30.0% (I+MLT) and 35.0% (I/R+MLT) and blastocyst yield to 17.5% and 25.0%, although most values remained below sham levels. A single melatonin dose therefore partially preserves the fertilizing and embryo-supporting capacity of spermatozoa after testicular ischemic injury.

Background/Objectives: Although vitamin K has been implicated in osteoarthritis pathophysiology, the specific effects of vitamin K2 (menaquinone) on cartilage degeneration remain poorly characterized. This study aimed to investigate the effect of oral vitamin K2 supplementation in a monosodium iodoacetate-induced osteoarthritis model. Methods: Twenty-four male Sprague Dawley rats were included in the study and divided into 3 equal groups: sham group, control (osteoarthritis) group, and treatment group. Saline was applied to the right knee of the sham group, and MIA was applied intra-articularly to the right knee of the control and treatment groups to create an osteoarthritis model. Rats in the treatment group were given 8 micrograms (μg)/day of vitamin K2 orally in addition to the standard diet. After 28 days of follow-up, all rats were euthanized. The right knee articular cartilage was examined histologically with Hematoxylin–Eosin and Safranin O and immunohistochemically with type II collagen alpha 1 and Matrix Metalloproteinase-13. Results: Histological evaluation demonstrated significantly lower Mankin scores in the treatment group (4.25 ± 0.83) compared with the control group (11.10 ± 0.83). Immunohistochemical analysis showed more intense type II collagen staining and reduced matrix metalloproteinase-13 staining in the treatment group relative to the control group. Conclusions: Oral vitamin K2 administration was associated with reduced cartilage degeneration and improved matrix preservation at the 28-day endpoint in an induced MIA osteoarthritis rat model.