We investigated the morphologic and molecular effects of exposure to cadmium (Cd) for 30 and 60 days on the uteri of mice. We assessed uterine morphometric measurements, eosinophilia, mast cell numbers, endometrial apoptosis, proliferation and estrogen receptor alpha (ERα) immunoreactivity. We examined vaginal smears that reflected the hormonal alterations in the female reproductive tract. Because the female reproductive tract exhibits different morphology at each stage of the estrous cycle, we sacrificed all animals at estrus to make appropriate comparisons. Female BALB/c mice were exposed to 200 ppm Cd in their drinking water for either 30 or 60 days. Cd exposure caused significant decreases in endometrial thickness and number of glands in estrus phase uteri. The endometrial eosinophilia in the groups exposed to Cd also decreased compared to controls. Cd exposure increased the number of mast cells. Luminal and glandular epithelia were examined using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and by immunostaining proliferating cell nuclear antigen (PCNA) and estrogen receptor α (ERα). Compared to controls, the apoptotic index increased with time in both Cd exposed groups, while the proliferation index decreased. ERα immunoreactivity was decreased in both Cd exposed groups compared to controls; the decrease was most apparent in the 30 day Cd group. We found that 60 day Cd exposure increased apoptosis in the endometrium, which may affect the receptivity of the uterus for implantation.

We investigated the effects of ionizing radiation on maturation ability and radiosensitivity of oocytes enclosed in preantral and antral follicles. Balb/c female mice received total body single dose gamma radiation (7.2 Gy) at the diestrous to proestrous transition period. In the first experiment, spontaneously ovulated oocytes were collected from irradiated animals. In the second experiment, irradiated animals were allowed to superovulate to assess the ovarian function. The spontaneous ovulation rate of the follicles exposed at antral stage was significantly lower than the sham-irradiated mice (p < 0.01), and most of the oocytes were found at the metaphase I stage. Oocyte morphology and the ovulation rate of the follicles exposed at preantral stage were similar to the sham-irradiated group. Minimal morphological abnormalities were observed in the oocytes and the polar body as well. The superovulation response of all the irradiated animals was lower than the respective control animals. The superovulation rate was significantly lower in the first ovulation after irradiation (p < 0.01). In conclusion, our findings indicate that total body gamma irradiation, on a basis of estrous cycle stages, leads to ovulation failure in the antral stage while causes abnormal oocyte morphology in the preantral stage follicles in mice

Background and Objectives: Allergic contact dermatitis is a common type IV hypersensitivity reaction characterised by redness, itching, oedema and thickening of the skin. It occurs in about 7% of the population and its incidence is increasing. It has been observed that the preconditioning of tissues by exposing them to transient ischemia increases resistance to subsequent permanent ischemia, and this phenomenon is called ischemic preconditioning. It has been shown that conditioning in one organ can also protect other organs. The protective effect of remote ischemic preconditioning is thought to be based on the induction of anti-inflammatory responses. The aim of this project was to investigate the anti-inflammatory and antipruritic effects of remote ischemic postconditioning in a mouse model of experimental allergic contact dermatitis. Methods: Experimental allergic contact dermatitis was induced with 1-fluoro-2,4-dinitrobenzene. Remote ischemic postconditioning was performed at 3 and 25 h after the challenge. Ear thickness and number of scratches 24 and 48 h after challenge, as well as cytokine levels and the infiltration of mast cells, neutrophils, CD4⁺ and CD8⁺ T lymphocytes in serum and ear tissue at 48 h were measured to determine the effect of RIPsC. Results: Remote ischemic postconditioning decreased ear thickness, one of the symptoms of allergic contact dermatitis (p < 0.0001). It had no significant effect on the number of scratches. It reduced serum IL-17 levels (p < 0.01). It alleviated local inflammation by suppressing CD8⁺ T lymphocyte and neutrophil infiltration. Conclusions: It was concluded that remote ischemic postconditioning may alleviate the symptoms of allergic contact dermatitis by suppressing CD8⁺ T lymphocyte and neutrophil infiltration and reducing IL-17 secretion.

Background/Objectives: Acute kidney injury poses a significant public health concern, contributing to elevated rates of morbidity and mortality. In our study, we sought to explore the involvement of cation channels, known to influence renal physiology, in Rhabdomyolysis-Associated Acute Kidney Injury (RIAKI). Materials and Methods: A total of 32 Sprague–Dawley rats were divided into four groups for our study. All rats underwent 24 h of dehydration prior to experimentation. Subsequently, the control group received physiological saline, while the remaining groups (RIAKI-24, RIAKI-48, and RIAKI-72) were administered intramuscular injections of 5 mL/kg of 50% glycerol solution. The control and RIAKI-24 groups were euthanized 24 h post-injection, the RIAKI-48 group at 48 h, and the RIAKI-72 group at 72 h. Urine, blood, and renal tissue samples were collected for the assessment of renal function and histological damage. Results: Serum urea and creatinine levels exhibited a time-dependent increase, alongside reduced creatinine clearance. Moreover, kidney tissue analysis revealed elevated levels of TRPV1, TRPV4, and TRPC6 in the RIAKI-72 group compared to the control. The RIAKI-24 group displayed the most severe histological damage among the experimental groups. Conclusions: RIAKI was accompanied by changes in renal function and histopathology, as well as altered renal TRPV1, TRPV4, and TRPC6 protein levels. These findings suggest the potential involvement of TRP channels in RIAKI but do not establish their functional activity or whether the observed changes are harmful, protective, or compensatory. Further studies are needed to clarify the functional roles of these channels in renal injury.