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.

This study aimed to histopathologically investigate the protective effect of Eremurus spectabilis M. Bieb's on Cornu Ammonis (CA) in diethylnitrosamine (DEN)-induced neurotoxicity. In the study, rats were equally divided into (n=8); Control Group: Rats in this group were not exposed to any treatment, DEN Group: Rats in this group were treated with 150 mg DEN/kg body weight dissolved in 0.9% physiological water once a month and thioacetamide (TAA) 200 mg /kg body weight once a week intraperitoneally (i.p.), Lyophilized plant extract (LPE) Group: The rats in this group were given 150 mg DEN/kg once a month dissolved in 0.9% physiological water, 200 mg TAA/kg once a week and 100 mg/kg body weight LPE daily by oral gavage method and fed with standard rat chow and tap water, Nanoparticle plant extract (NPE) Group: Rats in this group were given 150 mg DEN/kg once a month and TAA 200 mg/kg once a week (i.p.) and 100 mg/kg body weight nanoparticle plant extract dissolved in 0.9% physiological water and fed with standard rat chow and tap water by oral gavage method. In our findings, a significant reduction in granular layer cells and significant dissociations in CA regions were observed in DEN group rats. There was a slight alleviation in the lesions in the groups to which we gave lyophilized plant extract. In rats treated with nanoparticle plant extract, CA gave an appearance very close to the control group. In conclusion, Eremurus spectabilis M. Bieb. may exhibit a protective effect against neurotoxicity as well as Alzheimer’s disease and Parkinson’s disease, which are closely associated with the CA regions. Also, it was reported as an important finding that the nanoparticle extract of E. spectabilis was more effective than the lyophilized extract. FULL TEXT PDF

In this case report, the aim was to contribute to understanding PNOE's clinical presentation, histopathological features, and successful treatment approaches, emphasizing the significance of accurate diagnosis and appropriate management in affected felines. Proliferative necrotic otitis externa (PNOE) is a very rare skin disease of unknown etiology affecting the vertical ear canal and the concave surface of the auricle, which may be accompanied by secondary yeast or bacterial infections. In this case 8-month-old Scottish fold shorthair cat has fragile, papillomatous growths and caseous purulent exudate in the ear canal was presented. The differential diagnosis of this condition includes otoacariasis, plasma cell pododermatitis, papillomavirus and chronic bacterial or yeast otitis externa. Despite antimicrobial and antiparasitic based previous treatments, the lesions persisted. Histopathological examination revealed acanthotic epidermis, necrotic keratinocytes, and inflammatory cell infiltrates. Treatment involved methylprednisolone injection, topical pomades, and systemic antibiotics. The cat showed improvement after initial treatment week, with regression of lesions and cessation of ear discharge. Follow-up visits demonstrated continued improvement, and after two months, minimal sequelae remained. In conclusion, despite the unknown etiology of PNOE, the disease is quite responsive to immunosuppressive therapy, which is beneficial for both diagnosis and treatment.