Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity.

This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist, (3 mg/kg i.p.) were administered to rats every day for 5 days. At the end of the study, kidney tissues were analysed using histological and biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, and glomerular adhesion in the Cd group. However, these lesions were significantly reduced in the Cd + Se and Cd + 2-APB groups, while the Cd + Se + 2-APB group showed a histological appearance similar to the control group. Immunohistochemical analysis revealed that Caspase-3, Bax, and TRPM2 expression was higher in the Cd group, while these levels were lower in the Se and 2-APB treatment groups (p < 0.05). Among the groups that received Cd, urea, creatinine, TOS, TNF-α, and IL-1β levels were at the highest level in the Cd group, while TAS level was at the lowest level (p < 0.05). The Se and 2-APB treatment modulated these parameters; however, Se + 2-APB treatment reduced urea, creatinine, TOS, TNF-α, and IL-1β levels to the lowest level compared to the Cd groups and brought the TAS level closer to the control group (p < 0.05). These findings indicated that targeting TRPM2 channel inactivation together with the selenium treatment could alleviate Cd-induced nephrotoxicity.

Background/Objective: Electromagnetic radiation (EMR) from wireless technologies has raised concerns about male reproductive health. We aimed to evaluate the protective role of alpha-lipoic acid (ALA), a potent antioxidant, against testicular alterations induced by 2.45 GHz EMR. Methods: Twenty-eight adult male rats were randomly divided into four groups: control, EMR, ALA, and ALA+EMR. Animals in the EMR and ALA+EMR groups were exposed to EMR for 2 h/day for 1 month. Testicular tissues were examined histologically, stereologically, and immunohistochemically, while serum samples were analysed biochemically. Results: EMR exposure caused marked structural damage, including disruption of seminiferous tubule architecture, increased collagen deposition, and expansion of tubular and interstitial volumes. These pathological changes were primarily prevented in the ALA+EMR group. Immunohistochemical analyses revealed increased IL-6 and TNF-α expression following EMR exposure, whereas ALA supplementation significantly reduced these inflammatory markers and restored AR, ZO-1, and ZO-2 expression. Biochemically, EMR reduced antioxidant enzyme activities (SOD, GSH, GPx) and elevated MDA levels, indicating oxidative stress; these parameters were reversed by ALA treatment. Conclusions: Collectively, our findings demonstrate that 2.45 GHz EMR induces oxidative stress, inflammation, and testicular injury, while ALA provides significant protection. These results highlight the therapeutic potential of ALA as a protective agent against EMR-related reproductive toxicity and infertility risk.

Purpose: Doxorubicin (DOXR) is frequently utilized as a standalone or in combination therapy for treating various cancer types. Despite well-known side effects that vary depending on the dose, the definitive effects on liver health are not fully clarified. This research aims to explore the role of the transient receptor potential melastatin-2 (TRPM2) channel in rats treated with DOXR, using N-(p-amylcinnamoyl) anthranilic acid (ACA) to inhibit it and examines the protective properties of selenium (Se) on hepatic tissues. Methods: Rats were allocated into six groups, each containing ten rats: control, DMSO, DOXR, DOXR + Se, DOXR + ACA, and DOXR + ACA + Se. Serum levels of AST, ALT, LDH, triglycerides, and total cholesterol were measured. Additionally, liver tissues were subjected to immunohistochemical tests and histopathological evaluations for TRPM2 channel, 8-OHdG, and caspase-3 (Casp-3) expressions. Results: Measurements in serum (AST, ALT, LDH, triglycerides, and total cholesterol) and liver expressions of 8-OHdG, TRPM2 channel, and Casp-3 were significantly elevated in the DOXR group compared to DOXR + Se, DOXR + ACA, and DOXR + ACA + Se groups (p < 0.05). Particularly, these biomarkers were significantly lower in groups treated with Se and ACA, compared to the DOXR-only group (p < 0.05), underscoring selenium's potential to mitigate DOXR-induced liver damage. Conclusions: The results suggest that the concurrent administration of Se and ACA with DOXR could be an effective therapeutic approach in combating DOXR-induced hepatotoxicity.