Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al³⁺ (7.5 mg/kg/day (0.15 LD₅₀) as AlCl₃ (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl⁻ control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD₅₀), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD₅₀), 21 days, i.g.). The treatment with AlCl₃ increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl₃ treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl₃ treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl₃ had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

In recent decades, a lot of attention has been paid to Cannabis sativa L. due to its useful applications, including in fibers, oil, food for humans and animals, and therapeutics. The present study aimed to determine antioxidant activity of cannabinoids in Cannabis sativa L. in vivo, evaluating the possible antioxidative effect of Cannabis sativa L. extract (CE) on malondialdehyde (MDA) and glutathione (GSH) concentrations as well as on catalase (CAT) activity in BALB/c mice. In total, 40 mice were divided into five equal groups: the aluminum group (7.5 mg AlCl₃/kg/d (0.15 LD₅₀), the saline group, the 10% ethanol group (an appropriate amount of the solution for mouse weight), the CE group (1.6 mg CE/g/day), and the aluminum-CE group (7.5 mg AlCl₃ plus 1.6 mg CE/g/day). The results of the study showed that CE significantly decreased (by 26.81%, p < 0.05) the concentration of GSH in blood of the mice and the concentration of MDA in the brain (by 82.12%) and liver (by 53.5%) of the mice compared to the respective concentrations in the AlCl₃ group. CE significantly (p < 0.05) increased CAT activity in the brain (by 64.79%) and liver (by 72.37%) of the mice after the AlCl₃-induced prooxidant effect. The results showed the antioxidant activity of cannabidiolic acid (CBDA) in vitro. The findings in vivo indicate that Cannabis sativa L. is a good source of natural antioxidants and can be used in the management of oxidative stress.

Selenium is an essential trace element that maintains normal brain function, mainly due its antioxidant properties. Although the amount of Se in the body is tightly regulated by the liver, both an excess of and deficiency in Se can modulate the cellular redox status and affect the homeostasis of other essential elements for both humans and animals. The aim of this study was to determine the effect of inorganic selenium excess on oxidative stress and iron homeostasis in brain and liver of laboratory BALB/c mice, which were supplemented with Na₂SeO₃ solution (0.2 mg and 0.4 mg Se/kg body weight) for 8 weeks. The content of the lipid peroxidation product malondialdehyde and antioxidant enzyme catalase activity/gene expression were used as markers of oxidative damage and were evaluated by spectrophotometric assays. Selenium and iron concentrations were determined by inductively coupled plasma mass spectrometry (ICP-MS). Catalase gene expression was analyzed by qRT-PCR and ΔΔCt methods. Our results showed that doses of 0.2 mg Se and 0.4 mg Se caused a relatively low accumulation of Se in the brain of mice; however, it induced a 10-fold increase in its accumulation in the liver and also increased iron accumulation in both tested organs. Both doses of Se increased the content of malondialdehyde as well as decreased catalase activity in the liver, while the 0.4 mg Se dose has also activated catalase gene expression. Brain of mice exposed to 0.2 mg Se showed reduced lipid peroxidation; however, the exposure to 0.4 mg of Se increased the catalase activity as well as gene expression. One may conclude that exposure to both doses of Se caused the accumulation of this micronutrient in mice brain and liver and have also provided a disrupting effect on the levels of iron. Both doses of Se have triggered oxidative liver damage. In the brain, the effect of Se was dose dependent, where −0.2 mg of Se provided antioxidant activity, which was observed through a decrease in lipid peroxidation. On the contrary, the 0.4 mg dose increased brain catalase activity as well as gene expression, which may have contributed to maintaining brain lipid peroxidation at the control level.

(1) In this study we determined the effect of long-term selenomethionine administration on the oxidative stress level and changes in antioxidant protein/enzyme activity; mRNA expression; and the levels of iron, zinc, and copper. (2) Experiments were performed on 4–6-week-old BALB/c mice, which were given selenomethionine (0.4 mg Se/kg b.w.) solution for 8 weeks. The element concentration was determined via inductively coupled plasma mass spectrometry. mRNA expression of SelenoP, Cat, and Sod1 was quantified using real-time quantitative reverse transcription. Malondialdehyde content and catalase activity were determined spectrophotometrically. (3) After long-term SeMet administration, the amount of Se increased by 12-fold in mouse blood, 15-fold in the liver, and 42-fold in the brain, as compared to that in the control. Exposure to SeMet decreased amounts of Fe and Cu in blood, but increased Fe and Zn levels in the liver and increased the levels of all examined elements in the brain. Se increased malondialdehyde content in the blood and brain but decreased it in liver. SeMet administration increased the mRNA expression of selenoprotein P, dismutase, and catalase, but decreased catalase activity in brain and liver. (4) Eight-week-long selenomethionine consumption elevated Se levels in the blood, liver, and especially in the brain and disturbed the homeostasis of Fe, Zn, and Cu. Moreover, Se induced lipid peroxidation in the blood and brain, but not in the liver. In response to SeMet exposure, significant up-regulation of the mRNA expression of catalase, superoxide dismutase 1, and selenoprotein P in the brain, and especially in the liver, was determined.

Oxidative stress is proposed in the literature as an important player in the development of CHF and correlates with left ventricle (LV) dysfunction and hypertrophy in the failing heart. In this study, we aimed to verify if the serum oxidative stress markers differ in chronic heart failure (CHF) patients’ groups depending on the LV geometry and function. Patients were stratified into two groups according to left ventricular ejection fraction (LVEF) values: HFrEF (<40% (n = 27)) and HFpEF (≥40% (n = 33)). Additionally, patients were stratified into four groups according to LV geometry: NG–normal left ventricle geometry (n = 7), CR–concentric remodeling (n = 14), cLVH–concentric LV hypertrophy (n = 16), and eLVF–eccentric LV hypertrophy (n = 23). We measured protein (protein carbonyl (PC), nitrotyrosine (NT-Tyr), dityrosine), lipid (malondialdehyde (MDA), oxidizes (HDL) oxidation and antioxidant (catalase activity, total plasma antioxidant capacity (TAC) markers in serum. Transthoracic echocardiogram analysis and lipidogram were also performed. We found that oxidative (NT-Tyr, dityrosine, PC, MDA, oxHDL) and antioxidative (TAC, catalase) stress marker levels did not differ between the groups according to LVEF or LV geometry. NT-Tyr correlated with PC (r_s = 0.482, p = 0.000098), and oxHDL (r_s = 0.278, p = 0.0314). MDA correlated with total (r_s = 0.337, p = 0.008), LDL (r_s = 0.295, p = 0.022) and non-HDL (r_s = 0.301, p = 0.019) cholesterol. NT-Tyr negatively correlated with HDL cholesterol (r_s = -0.285, p = 0.027). LV parameters did not correlate with oxidative/antioxidative stress markers. Significant negative correlations were found between the end-diastolic volume of the LV and the end-systolic volume of the LV and HDL-cholesterol (r_s = –0.935, p < 0.0001; r_s = –0.906, p < 0.0001, respectively). Significant positive correlations between both the thickness of the interventricular septum and the thickness of the LV wall and the levels of triacylglycerol in serum (r_s = 0.346, p = 0.007; r_s = 0.329, p = 0.010, respectively) were found. In conclusions, we did not find a difference in serum concentrations of both oxidant (NT-Tyr, PC, MDA) and antioxidant (TAC and catalase) concentrations in CHF patients’ groups according to LV function and geometry was found. The geometry of the LV could be related to lipid metabolism in CHF patients, and no correlation between oxidative/antioxidant and LV markers in CHF patients was found.

The aim of this study was to investigate the effects of aluminum (Al) or selenium (Se) on the “primary” antioxidant defense system enzymes (superoxide dismutase, catalase, and glutathione reductase) in cells of mouse brain and liver after long-term (8-week) exposure to drinking water supplemented with AlCl₃ (50 mg or 100 mg Al/L in drinking water) or Na₂SeO₃ (0.2 mg or 0.4 mg Se/L in drinking water). Results have shown that a high dose of Se increased the activities of superoxide dismutase and catalase in mouse brain and liver. Exposure to a low dose of Se resulted in an increase in catalase activity in mouse brain, but did not show any statistically significant changes in superoxide dismutase activity in both organs. Meanwhile, the administration of both doses of Al caused no changes in activities of these enzymes in mouse brain and liver. The greatest sensitivity to the effect of Al or Se was exhibited by glutathione reductase. Exposure to both doses of Al or Se resulted in statistically significant increase in glutathione reductase activity in both brain and liver. It was concluded that 8-week exposure to Se caused a statistically significant increase in superoxide dismutase, catalase and glutathione reductase activities in mouse brain and/or liver, however, these changes were dependent on the used dose. The exposure to both Al doses caused a statistically significant increase only in glutathione reductase activity of both organs.