Parkinson's disease is a progressive neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. The causes of Parkinson's disease are not fully understood; however, increasing evidence implicates oxidative stress. The study was aimed at assessing the nature of the changes in the oxidation-antioxidant balance in the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum in a rat model of Parkinson's disease (PD). Sixteen male Wistar rats were divided into 2 groups: Icontrol, IIParkinson's disease. The 8-weeks-old animals were decapitated, their brains removed and the following structures dissected and then frozen for further biochemical assays: cerebral cortex, striatum, hippocampus, thalamus and cerebellum. The activities of: the catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD) and the isoenzymes: Cu/ZnSOD and MnSOD; together with the malondialdehyde (MDA) and the total oxidative status (TOS) concentrations were measured in each structure. A significantly increased activities of SOD, Cu/ZnSOD, GST and reduced GR activity and an increase of MDA concentration were observed in the striatum of PD rats, comparing to the control group, combined with a significantly reduced activities of GR,SOD, Cu/ZnSOD and an increased GPX activity and MDA concentration in the hippocampus, a significantly lower GR, SOD, MnSOD, Cu/ZnSOD, and GST activities in the cerebral cortex. A significantly lower GR activity, higher CAT activity and MDA concentration in the thalamus and a significantly increased GR activity in the cerebellum were observed in PD rats compared to the corresponding control group. Oxidative stress in PD involves many brain structures and various antioxidant enzymes and oxidative status parameters become dysfunctional, depending on the area of the brain, which might reflect the complexity of the clinical symptoms of PD.

The adipose tissue, apart from storing energy, plays a role of an endocrine organ. One of the most important adipokines secreted by adipose tissue is adiponectin, which is also produced by cardiomyocytes and connective tissue cells within the heart. Adiponectin is known for its beneficial effect on the metabolism and cardiovascular system and its low level is a factor of development of many cardiovascular diseases. Paradoxically, in the course of heart failure, adiponectin level gradually increases with the severity of the disease and higher adiponectin level is a factor of poor prognosis. As a result, there is a growing interest in adiponectin as a marker of heart failure progression and a predictor of prognosis in the course of this disease.

Background and Objectives: Hypertrophic cardiomyopathy (HCM) depends on the primary impairment of sarcomeres, but it can also be associated with secondary alterations in the heart related to oxidative stress. The present study aimed to examine oxidative-antioxidant disturbances in patients with HCM compared with control individuals. Materials and Methods: We enrolled 52 consecutive HCM patients and 97 controls without HCM. The groups were matched for age, body mass index, and sex. Peripheral blood was collected from all patients to determine the total antioxidant capacity (TAC), total oxidant status (TOS), lipid hydroperoxide (LPH), and malondialdehyde (MDA). The oxidative stress index (OSI) was defined as the ratio of the TOS level to the TAC level. Results: The median age was 52 years, and 58.4% were female. The area under the curve (AUC) indicated good predictive power for the TAC and TOS [AUC 0.77 (0.69–0.84) and 0.83 (0.76–0.90), respectively], as well as excellent predictive power for the OSI [AUC 0.87 (0.81–0.93)] for HCM detection. Lipid peroxidation markers also demonstrated good predictive power to detect HCM patients [AUC_LPH = 0.73, AUC_MDA = 0.79]. Conclusions: The TOS, the TAC, LPH levels, and MDA levels have good predictive power for HCM detection. The holistic assessment of oxidative stress by the OSI had excellent power and could identify patients with HCM.

Heart failure (HF) is a common condition and one of the main morbidity and mortality factors in elderly patients. The incidence of HF progressively increases with age, reaching >10% in those aged 70 years or over. In the elderly population, both the diagnosis and the management of HF prove challenging, often requiring specialized care and a multidisciplinary approach. In seniors, atypical presentation of HF is much more common than in younger patients; thus, a holistic assessment with biomarkers related to HF allows for early diagnosis and accurate risk stratification in this group of patients. This article reviews the clinical and diagnostic differences in elderly patients with HF, highlighting the presence of comorbidities, frailty, cognitive impairment, and polypharmacy, as well as discussing potential biomarkers that may have clinical application in this population.

Propofol is an intravenous sedative-hypnotic agent that is commonly used to induce and maintain general anaesthesia. This drug has antioxidant properties, which are partly caused by a phenolic structure similar to α-tocopherol. The present study aimed to evaluate the effect of propofol on the level of oxidative stress biomarkers in the frontal cortex, striatum, thalamus, hippocampus and cerebellum in rats with experimental Parkinson's disease (PD). The experiment was performed on 24 male Wistar rats assigned to the following groups: 1 - control; 2 - PD; 3 - PD with propofol. The dopaminergic systems were damaged with 6-hydroxydopamine (6-OHDA) administered to each lateral ventricle (2x15 μg/5 μl). 60 mg/kg of propofol was later given to the 8-week-old rats intraperitoneally. The activities of superoxide dismutase (SOD) and its enzymes Cu/ZnSOD and MnSOD, together with the malondialdehyde (MDA) concentration, total oxidative status (TOS) and total antioxidant capacity (TAC), were measured. In the 2nd group, a significant increase in MDA concentration in the striatum, hippocampus and thalamus, and an increase of TOS in the striatum, thalamus and cerebellum were noted, along with a TAC decrease in the cortex, striatum and thalamus. Propofol caused a significant decrease in MDA levels in the cortex, striatum, hippocampus and thalamus, and a decrease in TOS levels in the cortex, striatum and cerebellum, with increased TAC in all evaluated structures. A shortage of natural antioxidants is observed in PD, along with an increase in pro-oxidants in many brain areas. Propofol inhibits oxidative stress in the brain, which shows its neuroprotective properties against oxidative damage.

Anabolic–androgenic steroids (AAS) are synthetic derivatives of testosterone that are used therapeutically but are frequently abused by athletes and individuals seeking to increase muscle mass. Their anabolic (promoting muscle growth) and androgenic (inducing masculine characteristics) effects result from androgen receptor activation in target tissues. However, chronic supraphysiological AAS exposure is associated with serious cardiovascular consequences, ranging from hypertension and lipid disorders to cardiomyopathy, atherosclerosis, and sudden cardiac death. This review provides an updated and integrative perspective on both the molecular and clinical aspects of AAS-induced cardiovascular toxicity, highlighting recent advances in understanding endothelial injury, oxidative stress, fibrosis, and arrhythmogenesis. Importantly, it emphasizes the emerging recognition of AAS abuse as a modifiable cardiovascular risk factor and discusses potential preventive and therapeutic strategies, including early cardiovascular screening and risk stratification. Understanding these mechanisms is essential for recognizing the clinical manifestations of AAS misuse and for improving cardiovascular risk assessment in affected individuals. These insights underscore the clinical significance of AAS abuse as a cardiovascular risk factor and the need for vigilant cardiac monitoring and early intervention in this population.