Objective: The increasing use of electronic devices, accompanied by advancing technologies, has led to heightened exposure to non-ionizing electromagnetic radiation (EMR). This exposure instigates the accumulation of free radicals and oxidative damage in tissues, consequently impacting biological systems. Notably, the testis is among the tissues adversely affected by EMR. Numerous studies have highlighted the pivotal role of the testis in sperm production, emphasizing the potential implications of any damage on the reproductive system. This study aims to assess the levels of lipid peroxidation through histological evaluation in the testicular tissue of prepubertal male rats exposed to electromagnetic radiation at varying electric field intensities within the 2.45 GHz radiofrequency (RF) range. Methods: The experimental group comprises six subdivisions, including a sham control group, as well as groups exposed to varying electric field strengths (EFS) of 0.6 V/m, 1.9 V/m, 5 V/m, 10 V/m, and 15 V/m, respectively. Excluding the sham control group, the remaining subgroups were subjected to a daily 2.45 GHz RF exposure for 1 hour starting immediately after fertilization. This exposure to different electric field intensities continued for 45 days post-birth. Results: The samples obtained from the RF radiation-exposed rats exhibited elevated malondialdehyde (MDA) values and decreased glutathione (GSH) values in the testicular tissue. Furthermore, a comparative analysis between the microwave radiation-exposed group and the control group revealed distinct histological alterations in the testicular tissue. Conclusion: In conclusion, our findings indicate that exposure to microwave radiation at an electric field intensity of 15 V/m can lead to significant histopathological and oxidative parameter changes in Wistar rats. These results underscore the potential effects of such exposure on human health.

Neurological impairments are the leading cause of post-stroke mortality, while stroke-related cardiovascular diseases rank second in significance.This study investigates the potential protective effects of MitoTEMPO (2,2,6,6-tetramethyl-4-[[2-(triphenylphosphonio) acetyl] amino]-1-piperidinyloxy, monochloride, monohydrate), a mitochondria-specific antioxidant, against cardiac and neurological complications following stroke. The objective is to assess whether MitoTEMPO can be utilized as a protective agent for individuals with a high risk of stroke. 17-week-old male Wistar Albino rats were randomly assigned to three groups: SHAM, ischemia-reperfusion (IR), and MitoTEMPO + ischemia-reperfusion (MT + IR; MitoTEMPO injection 0.7 mg/kg/day for 14 days). The SHAM group underwent a sham operation, while the IR group underwent 1-hour middle cerebral artery occlusion (MCAO) followed by 3 days of reperfusion. Afterwards, noninvasive thoracic electrical bioimpedance (TEB) and electrocardiography (ECG) measurements were taken, and sample collection was performed for histological and biochemical examinations. Our TEB and ECG findings demonstrated that MitoTEMPO exhibited a protective effect on most parameters affected by IR compared to the SHAM group. Furthermore, our biochemical and histological data revealed a significant protective effect of MitoTEMPO against oxidative damage. The findings suggest that both IR-induced cardiovascular abnormalities and the protective effect of MitoTEMPO may involve G-protein coupled receptor (GPCR)-mediated signaling mechanisms. This study was conducted with limitations including a single gender, a uniform age group, a specific stroke model limited to MCA, and pre-scheduled only one IR period. In future studies, addressing these limitations may enable the implementation of preventive measures for individuals at high risk of stroke.

Cardiac dysfunction is secondary to acute mesenteric ischemia (AMI) and abdominal aortic aneurysms (AAA). The underlying cause of distant organ damage in the heart is the formation of oxidative stress caused by ischemia-reperfusion. In this study, we investigated the possible protective effects of a novel mitochondria-targeted antioxidant MitoTEMPO on contractile dysfunction and structural defects of the rat papillary muscle caused by abdominal ischemia-reperfusion (AIR). In the experiments, adult Wistar-Albino rats were used and animals were divided randomly into 3 groups; sham-operated group (SHAM), an IR group that had aortic cross-clamping for 1 h followed by 2 h reperfusion, and a third group that received protective 0.7 mg/kg/day MitoTEMPO injection for 28-day before IR. As a result, it was observed that MitoTEMPO injection had a protective effect on the mechanical activities and structural properties of the papillary muscle impaired by AIR. Our study also showed that AIR disrupted the contractile function of the papillary muscle for each stimulation frequency and post-potentiation responses tested. This is common for each measured and calculated mechanical parameter and MitoTEMPO injection showed its protective effects. Consequently, calcium homeostasis seems to be impaired by AIR, and MitoTEMPO may exert its protective effect through energy metabolism by directly targeting the mitochondria.

Objective: Diabetes Mellitus (DM) not only causes hyperglycemia but also leads to clinical challenges involving respiratory functional impairments. The contraction of the diaphragm reduces pleural pressure, thereby contributing significantly to the process of breathing. This study examines the functional impairments in diaphragm muscle isometric contraction parameters due to increased reactive oxygen species (ROS) associated with DM, as well as the effects of MitoTEMPO, a mitochondria-specific antioxidant, on these impairments. Methods: Wistar Albino male rats at 12-14 weeks of age were randomly divided into three groups: the control group (CON, n=6), the diabetes group (DM, n=6), and the diabetes + MitoTEMPO (MT, n=6) group. A single dose of 50 mg/kg streptozotocin (STZ) was administered to the rats in the DM and MT groups. When the rats in the MT group reached a blood glucose level of 300 mg/dl, they were administered MitoTEMPO at a dose of 0.7 mg/kg/day for 28 days. Isometric contraction recordings were obtained from diaphragm muscle preparations isolated from the experimental animals at the end of the 28-day period. Results: Although the effectiveness of mitochondria-specific antioxidants in reducing blood glucose levels in DM is debated in the literature, results for the MT group were interestingly indicative of a statistically significant decrease in blood glucose levels following MitoTEMPO administration at the end of the fourth week. Furthermore, MitoTEMPO exhibited therapeutic effects on diaphragm muscle contraction parameters impaired by DM. Conclusion: The findings suggest that in DM patients, MitoTEMPO could be utilized for blood glucose control and might also be effective in the treatment of DM-induced diaphragm muscle mechanical dysfunction.

Protective vs. Therapeutic Effects of Mitochondria-Targeted Antioxidant MitoTEMPO on Rat Sciatic Nerve Crush Injury: A Comprehensive Electrophysiological Analysis. Peripheral nerve injuries often result in long-lasting functional deficits, prompting the need for effective interventions. MitoTEMPO (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl) triphenylphosphonium chloride) is a mitochondria-targeted antioxidant that has shown protective and therapeutic effects against pathologies associated with reactive oxygen species. This study explores the utilization of MitoTEMPO as a therapeutic and protective agent for sciatic nerve crush injuries. By employing advanced mathematical approaches, the study seeks to comprehensively analyze nerve conduction parameters, nerve excitability, and the distribution of nerve conduction velocities to gauge the potential. Forty Wistar-Albino rats were randomly divided into following groups: (I) SHAM—animals subjected to sham operation and treated intraperitoneally (i.p.) with vehicle (bidistilled water) for 14 days; (II) CI (crush injury)—animals subjected to CI and treated with vehicle 14 days; (III) MiP—animals subjected to 7 days i.p. MitoTEMPO treatment before CI (0.7 mg/kg/day dissolved in vehicle) and, only vehicle for 7 days after CI, protective MitoTEMPO; and (IV) MiT—animals i.p. treated with only vehicle for 7 days before CI and 7 days with MitoTEMPO (0.7 mg/kg/day dissolved in vehicle) after CI, therapeutic MitoTEMPO. Nerve excitability parameters were measured, including rheobase and chronaxie, along with compound action potential (CAP) recordings. Advanced mathematical analyses were applied to CAP recordings to determine nerve conduction velocities and distribution patterns. The study revealed significant differences in nerve excitability parameters between groups. Nerve conduction velocity was notably reduced in the MiP and CI groups, whereas CAP area values were diminished in the MiP and CI groups compared to the MiT group. Furthermore, CAP velocity was lower in the MiP and CI groups, and maximum depolarization values were markedly lower in the MiP and CI groups compared to the SHAM group. The distribution of nerve conduction velocities indicated alterations in the composition of nerve fiber groups following crush injuries. In conclusion, postoperative MitoTEMPO administration demonstrated promising results in mitigating the detrimental effects of nerve crush injuries.