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.

In this study, the genetic diversity was investigated among 12 soybeans genotypes using inter simple sequence repeats (ISSR) and agronomic traits. DNA was isolated from the leaves of the genotypes. For molecular characterization, a total of 26 primers of ISSRs and eight agronomic characteristics were evaluated. ISSR analysis revealed 88 polymorphic bands. The genetic diversity among the genotypes according to ISSR analysis and agronomic traits were estimated based on Nei homology and Euclidian distance, respectively, and dendrograms reflecting genetic similarity were constructed using UPGMA and NTSYSpc, respectively. Nei’s homology coefficient values used for ISSR analysis ranged from 78%-84%, and the average Euclidean distance used for agronomic data ranged from 1.96-9.77. Although soybean genotypes evaluated in this study were highly similar, dendrograms showed that these genotypes could be distinguished both morphologically and genetically.

Background/Objectives: Diabetic cardiomyopathy (DCM) is largely driven by severe oxidative stress and calcium dyshomeostasis. We examined the targeted antioxidant and therapeutic effects of zinc sulfate (ZnSO₄) on contractile dynamics, oxidative damage, calcium turnover, and apoptosis/fibrosis in aged female rats with type 2 diabetes. Methods: Thirty-two aged female Wistar rats were divided into Control, Control + ZnSO₄, Diabetes (DM), and DM + ZnSO₄ groups. DM was induced via high-fat diet and 30 mg/kg streptozotocin. After a 4-week complication period, treatment groups received 10 mg/kg/day ZnSO₄ (i.p.) for 6 weeks. Left ventricular papillary muscle contraction, oxidative/antioxidant markers (MDA/GSH), and gene expressions (SIRT1, GLUT4, SERCA2a, RyR2, Cav1.2, PLN) were evaluated. Myocardial architecture, fibrosis, and apoptosis were analyzed immunohistochemically. In DM rats, contractile force (CF) and velocities (±dF/dtmax) significantly declined. Results: Concurrently, SIRT1, GLUT4, SERCA2a, RyR2, Cav1.2, and antioxidant GSH decreased, while oxidative lipid damage (MDA), PLN, Caspase-3 activity, Collagen I, and fibrosis increased (p < 0.001). ZnSO₄ treatment in diabetic rats acted as a potent antioxidant modulator; it restored redox balance, activated the SIRT1/GLUT4 pathway, protected calcium-handling proteins from oxidative degradation, and significantly improved contractile dynamics. It also preserved myocardial architecture by reducing apoptosis and fibrosis. In healthy rats, ZnSO₄ caused mild stress and early fibrosis. Conclusions: In conclusion, while inducing mild stress in healthy myocardium, zinc supplementation provides robust antioxidant protection in diabetic hearts. It activates SIRT1, suppresses oxidative damage, maintains calcium homeostasis, and restores contractile dynamics, demonstrating strong antioxidant therapeutic potential against DCM.