Decrease In Catalase Activity Research Articles

Chronic Oral Administration of Aluminum Hydroxide Stimulates Systemic Inflammation and Redox Imbalance in BALB/c Mice.

The present study is aimed at investigating the long-term effects of the aluminum hydroxide administration in the small intestine, lung, liver, and kidney of male BALB/c mice. The mice received via orogastric gavage phosphate buffered or 10 mg/kg aluminum hydroxide 3 times a week for 6 months. Administration of aluminum hydroxide decreased hemoglobin, hematocrit, and erythrocyte. In the blood, kidney and liver function markers were evaluated, and long-term administration of aluminum hydroxide led to an increase in AST levels and a decrease in urea levels. The animals exposed to aluminum showed higher lipid and protein oxidation in all the organs analyzed. In relation to the enzymes involved in antioxidant defense, the lungs showed lower superoxide dismutase (SOD) and catalase activity and a lower reduced and oxidized glutathione (GSH/GSSG) ratio. In the liver, aluminum administration led to a decrease in catalase activity and the GSH/GSSG ratio. Lower catalase activity was observed in the small intestine, as well as in the lungs and liver. In addition to alterations in antioxidant defense, increased levels of the chemokine CCL-2 were observed in the lungs, lower levels of IL-10 in the liver and small intestine, and decreased levels of IL-6 in the intestine of the animals that received aluminum hydroxide for 6 months. Long-term exposure to aluminum promoted steatosis in the liver. In the kidneys, mice treated with aluminum presented a decreased glomerular density than in the naive control group. In the small intestine, exposure caused villi shortening. Our results indicate that long-term oral administration of aluminum hydroxide provokes systemic histological damage, inflammation, and redox imbalance.

Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity

Cuprizone (CPZ) is a neurotoxic agent that is used to induce demyelination and neurotoxicity in rats. This study aimed to investigate the protective potential of sulforaphane (SF), nuclear factor E2 related factor (Nrf-2) activator, against CPZ-induced cardiotoxicity and hepatotoxicity. Male adult Wistar rats (n = 18) were fed with a regular diet or a CPZ-contained diet (0.2%) for four weeks. The rats were divided into three groups (n = 6): negative control rats, CPZ-exposed rats, and CPZ + SF treated rats. SF was intraperitoneally administrated (2 mg/kg/day) for two weeks. The anti-inflammatory and anti-oxidative functions of SF were investigated biochemically, histologically, and immunohistochemically. CPZ increased serum levels of cardiac troponin 1 (CTn1), aspartate amino transaminase (AST), alanine amino transaminase (ALT), and alkaline phosphatase (ALP). In addition, serum levels of inflammatory interferon-gamma (IFN-γ), and pro-inflammatory interleukin 1β (IL-1β) were significantly elevated. Moreover, CPZ administration provoked oxidative stress as manifested by declined serum levels of total antioxidant capacity (TAC), as well as, stimulated lipid peroxidation and decreased catalase activities in both cardiac and hepatic tissues. SF treatment reversed all these biochemical alterations through exerting anti-oxidative and anti-inflammatory activities, and this was supported by histopathological investigations in both cardiac and hepatic tissues. This SF-triggered modulation of oxidative stress and inflammation is strongly associated with Nrf-2 activation, as evidenced by activated immunoexpression in both cardiac and hepatic tissues. This highlights the cardioprotective and hepatoprotective activities of SF via Nrf-2 activation and enhancing catalase function.

GK-1 Induces Oxidative Stress, Mitochondrial Dysfunction, Decreased Membrane Potential, and Impaired Autophagy Flux in a Mouse Model of Breast Cancer.

Breast cancer (BC) is the second most common cancer worldwide in women. During the last decades, the mortality due to breast cancer has progressively decreased due to early diagnosis and the emergence of more effective new treatments. However, human epidermal growth factor receptor 2 (HER2) and triple-negative breast cancer (TNBC) remain with poor prognoses. In our research group, we are proposing the GK-1 immunomodulatory peptide as a new alternative for immunotherapy of these aggressive tumors. GK-1 reduced the growth rate of established tumors and effectively reduced lung metastasis in the 4T1 experimental murine model of breast cancer. Herein, the effect of GK-1 on the redox state, mitochondrial metabolism, and autophagy of triple-negative tumors that can be linked to cancer evolution was studied. GK-1 decreased catalase activity, reduced glutathione (GSH) content and GSH/oxidized glutathione (GSSG) ratio while increased hydrogen peroxide (H2O2) production, GSSG, and protein carbonyl content, inducing oxidative stress (OS) in tumoral tissues. This imbalance between reactive oxygen species (ROS) and antioxidants was related to mitochondrial dysfunction and uncoupling, characterized by reduced mitochondrial respiratory parameters and dissipation of mitochondrial membrane potential (ΔΨm), respectively. Furthermore, GK-1 likely affected autophagy flux, confirmed by elevated levels of p62, a marker of autophagy flux. Overall, the induction of OS, dysfunction, and uncoupling of the mitochondria and the reduction of autophagy could be molecular mechanisms that underlie the reduction of the 4T1 breast cancer induced by GK-1.

The catalase-peroxidase PiCP1 plays a critical role in abiotic stress resistance, pathogenicity and asexual structure development in Phytophthora infestans.

Catalase-peroxidase is a heme oxidoreductase widely distributed in bacteria and lower eukaryotes. In this study, we identified a catalase-peroxidase PiCP1 (PITG_05579) in Phytophthora infestans. PiCP1 had catalase/peroxidase and secretion activities and was highly expressed in sporangia and upregulated in response to oxidative and heat stresses. Compared with wild type, PiCP1-silenced transformants (STs) had decreased catalase activity, reduced oxidant stress resistance and damped cell wall integrity. In contrast, PiCP1-overexpression transformants (OTs) demonstrated increased tolerance to abiotic stresses and induced the upregulation of PR genes in the host salicylic acid pathway. The high concentration of PiCP1 can also induced callose deposition in plant tissue. Importantly, both STs and OTs have severely reduced sporangia formation and zoospore releasing rate, but the sporangia germination rate and type varied depending on environmental conditions. Comparative sequence analyses show that catalase-peroxidases are broadly distributed and highly conserved among soil-borne plant parasitic oomycetes, but not in freshwater-inhabiting or strictly plants-inhabiting oomycetes. In addition, we found that silencing PiCP1 downregulated the expression of PiCAT2. These results revealed the important roles of PiCP1 in abiotic stress resistance, pathogenicity and in regulating asexual structure development in response to environmental change. Our findings provide new insights into catalase-peroxidase functions in eukaryotic pathogens.

Chemotherapy Drugs Act Differently in the Expression and Somatic Mobilization of the mariner Transposable Element in Drosophila simulans.

Transposable elements (TEs) are abundant in genomes. Their mobilization can lead to genetic variability that is useful for evolution, but can also have deleterious biological effects. Somatic mobilization (SM) has been linked to degenerative diseases, such as Alzheimer's disease and cancer. We used a Drosophila simulans strain, in which SM can be measured by counting red spots in the eyes, to investigate how chemotherapeutic agents affect expression and SM of the mariner TE. Flies were treated with Cisplatin, Dacarbazine, and Daunorubicin. After acute exposure, relative expression of mariner was quantified by RT-qPCR and oxidative stress was measured by biochemical assays. Exposure to 50 and 100 µg/mL Cisplatin increased mariner expression and ROS levels; catalase activity increased at 100 µg/mL. With chronic exposure, the number of spots also increased, indicating higher mariner SM. Dacarbazine (50 and 100 µg/mL) did not significantly alter mariner expression or mobilization or ROS levels, but decreased catalase activity (100 µg/mL). Daunorubicin (25 and 50 µM) increased mariner expression, but decreased mariner SM. ROS and catalase activity were also reduced. Our data suggest that stress factors may differentially affect the expression and SM of TEs. The increase in mariner transposase gene expression is necessary, but not sufficient for mariner SM.

CATALASE ACTIVITY IN INTERACTION WITH IONIZED WATER AND OTHER ANTIOXIDANTS IN BLOOD PLASMA, LIVER, AND KIDNEY OF THE RAT DURING HYPERTHERMIC STRESS

The similarity between the responses seen after heat stress and those happening in the condition of oxidative stress suggests that heat stress is an environmental element that stimulates the generation of reactive oxygen species (ROS). Alkaline water, also known as ionized or reduced water (ERW), is water that has undergone electrochemical activation and has a pH greater than 7. The ERW also has excellent redox properties and other reducing features. ERW mimics the activity of the antioxidant enzyme, such as catalase (CAT) by scavenging ROS. The aim of this study was to examine the catalase activity in interaction with ERW under hyperthermic stress by including non-enzymatic antioxidants, glutathione, and vitamin C. White laboratory Young female Wistar rats weighing 180–220 g were divided into three groups of 15 for the experiment. Oxidative stress was caused by 41°C acute hyperthermic exposure. The first group is referred to as the control group (CPM), the second group is referred to as the ionized water treatment (TAM), and the third group is referred to as the ionized water treatment with added glutathione and vitamin C (TAD). The treatment period lasted 21 days. The treatment applied respectively to each group during the period of hyperthermic exposure caused a significant difference in CAT activity in blood plasma among the three groups. Liver CAT activity was increased in all three groups. Treatment for 21 days in all three groups led to a decrease in CAT activity in the blood plasma and in the kidneys. Acute hyperthermic exposure on the 21st day in the CPM and TAD groups for blood plasma has a statistically significant difference (p < 0.01). Also, in both the TAM and TAD groups there is a statistically significant difference (p < 0.01) in CAT activity, which is in contrast to the difference in the liver and kidney CAT activity between the remaining compared groups, which was shown to be statistically insignificant.

EFFECT OF STIMULATING ORGANISM WITH BACTERIAL LIPOPOLYSACCHARIDE ON DEVELOPMENT OF OXIDATIVE STRESS IN BICEPS FEMORIS OF RAT UNDER MODELLED METABOLIC SYNDROME

Metabolic syndrome is one of the most widespread non-infectious pathologies in the world. Metabolic syndrome is quite often accompanied by an increase in body weight and can lead to the development of type 2 diabetes. Between 1990 and 2015, global mortality associated with high body mass index increased by 28.3%.
 The purpose of this work is to determine the activity of antioxidant enzymes, the production of superoxide anion radical, the content of oxidatively modified proteins and the concentration of malondialdehyde in the biceps femoris of rats under experimental metabolic syndrome and stimulation of the organism with bacterial lipopolysaccharide.
 The study was conducted on 24 sexually mature male Wistar rats weighing 200-260 g. The animals were divided into 4 groups of 6 animals each. The first group was the control group. The second group was the test metabolic syndrome group. Metabolic syndrome was modelled by using a 20% fructose solution as the only source of water for 60 days. The third group received S. typhi bacterial lipopolysaccharide in the first week in a dose of 0.4 μg/kg intraperitonealy three times a week, then once a week throughout the experiment. The fourth group underwent the combined exposure to lipopolysaccharide and metabolic syndrome. The development of oxidative stress was observed in the three experimental groups. During modelling of the metabolic syndrome, oxidative stress was characterized by an increase in the production of the superoxide anion radical whilst the activity of the studied antioxidant enzymes decreased. During bacterial lipopolysaccharide stimulation, oxidative stress was characterized by an increase in the production of superoxide anion radical under an increase in superoxide dismutase activity and a decrease in catalase activity. Combined stimulation of the organism by bacterial lipopolysaccharide and modelled metabolic syndrome on the oxidative stress was characterized by an increase in the production of the superoxide anion radical under an increase in the activity of the studied antioxidant enzymes.
 The combined stimulation by bacterial lipopolysaccharide and modelled metabolic syndrome leads to the development of oxidative damage to the lipid and protein components of biceps femoris that is a consequence of an increase in the production of reactive oxygen species under a compensatory increase in the activity of antioxidant enzymes.

Thiazolidin-4-one prevents against memory deficits, increase in phosphorylated tau protein, oxidative damage and cholinergic dysfunction in Alzheimer disease model: Comparison with donepezil drug

Alzheimer’s disease (AD) is characterized mostly by memory decline. The current therapeutic arsenal for treating AD is limited, and the available drugs only produce symptomatic benefits, but do not stop disease progression. The search for effective therapeutic alternatives with multitarget actions is therefore imperative. One such a potential alternative is thiazolidin-4-one, a compound that exhibits anti-amnesic, anticholinesterase, and antioxidant activities. The aim of this study was evaluated the effects of 2-(4-(methylthio)phenyl)− 3-(3-(piperidin-1-yl)propyl) thiazolidin-4-one (DS12) on memory and neurochemical parameters in a model of AD induced by an intracerebroventricular injection of streptozotocin (STZ). Adult male rats were divided into five groups: I, control (saline); II, DS12 (10 mg/kg); III, STZ; IV, STZ + DS12 (10 mg/kg); V, STZ + donepezil (5 mg/kg). The rats were orally treated with DS12 and donepezil for a period of 20 days. Memory, acetylcholinesterase (AChE) activity, phosphorylated tau protein levels and oxidative stress were analyzed in the cerebral cortex, hippocampus, and cerebellum. Biochemical and hematological parameters were evaluated in the blood and serum. Memory impairment and the increase in AChE activity and phosphorylated tau protein level induced by STZ were prevented by DS12 and donepezil treatment. Streptozotocin induces an increase in reactive oxygen species levels and a decrease in catalase activity in the hippocampus, cerebral cortex, and cerebellum. DS12 treatment conferred protection from oxidative alterations in all brain structures. No changes were observed in serum biochemical parameters (glucose, triglycerides, cholesterol, uric acid, and urea) or hematological parameters, such as platelets, lymphocytes, hemoglobin, hematocrit, and total plasma protein. DS12 improved memory and neurochemical changes in an AD model and did not show toxic effects, suggesting the promising therapeutic potential of this compound.

Розвиток оксидативного стресу у лабораторних щурів за алкогольної інтоксикації

Introduction: the imbalance between the formation of reactive oxygen species (ROS) and the ability of cells to neutralize them is characterized as oxidative stress and occurs in almost any pathological condition. Reactions to convert ethanol to acetic acid are accompanied by an increase in ROS production. Given the prevalence of alcohol abuse and the contribution of oxidative stress to the development of pathological conditions, we formulated the aim of our work: to assess the impact of chronic alcohol intoxication on the development of oxidative stress in the mucous membranes of the digestive tract, liver, serum and bone of laboratory rats. Materials and Methods: the experiment was performed on 2-month-old rats of both sexes. The method of alcoholization is “semi-voluntary”. The experimental groups were given ethanol with 5 % drinking water at the beginning of the experiment and gradually increased to 15 %. The duration of the experiment is 108 days. Catalase activity (a marker of the antioxidant system) and malonic dialdehyde content (an indicator of the degree of lipid peroxidation) were determined in the serum, liver, jaw bone, mucous membranes of the mouth, stomach, small intestine, and colon of rats. The antioxidant-prooxidant index was calculated from the values ​​of these indicators. Results: prolonged consumption of alcohol by males and females led to a decrease in catalase activity in the tissues of the digestive tract from 16.0 % in the large intestinal to 25.0 % in the small intestinal mucosa, and, conversely, to increase in the jaws. the mucous membrane of the oral cavity and liver increased by 1.2–38.6 %. Chronic alcohol consumption increased the concentration of malonic dialdehyde in the mucous membranes of the gastrointestinal tract by 20.3–96.6 %, in serum – by 20.4–33.3 %, bone tissue – by 44.8–58.7 %. The balance between antioxidants and prooxidants in tissues most clearly reflects the antioxidant-prooxidant index. Alcohol consumption contributed to the reduction of antioxidant-prooxidant index in the tissues of the digestive tract by 37.6–65.0 %, in the liver by 24.7 %, in serum by 38.3 %, in the jaws by 4.2–15.9 %. In the mucous membrane of the oral cavity, this figure increased by 6.0–10.0 %. Conclusions: According to the results of our study, oxidative stress induced by ethanol developed to a greater extent in the mucous membrane of the small intestine, and to a lesser extent – in the mucous membrane of the mouth and jaw bone. Female tissues are more resistant to the development of oxidative stress due to prolonged alcohol consumption.

Зміна окремих показників еритроцитів крові щурів за впливу гістаміну і кверцетину

Зміна окремих показників еритроцитів крові щурів за впливу гістаміну і кверцетину

Catalase post-translational modifications as key targets in the control of erythrocyte redox homeostasis in children with obesity and insulin resistance.

Insulin resistance (IR) is the most common metabolic disturbance in children with obesity. Children with obesity and insulin resistance (ObIR+) display a detriment in erythroid antioxidant defenses, caused by an impaired catalase activity and the increase in oxidative and pro-inflammatory markers. Therefore, erythrocytes from ObRI+are more vulnerable to any oxidative stress elicitor. Since catalase is one of the erythrocytes' first antioxidant defenses, we intended to delve into the mechanisms underlying catalase's impaired activity. Given the lack of cellular organelles in erythrocytes, which prevents protein synthesis, we aimed study catalase post-translational modifications (PTMs) as targets of pro-inflammatory and pro-oxidant status of these cells in children with obesity and IR. Catalase levels of O-glycosylation, tyrosine nitration and S-glutathionylation were analyzed by Western blotting (WB) using immunoprecipitated catalase (IP-CAT) from erythrocyte lysates. Furthermore, Catalase was also identified by LC-MS/MS after isolation and enrichment of erythrocyte nitrosated proteins with a biotin switch approach. The results obtained suggest that catalase inhibition seen in children with obesity is partly due to the increase in the S-nitrosation of the enzyme. Indeed, exogenous administration of nitric oxide (NO) to cultured erythrocytes resulted in a decrease in catalase activity in all groups. Signals of other PTMs (O-glycosylation, Tyr-nitration and S-glutathionylation) were also detected in the erythrocyte catalase in every groups, although levels of catalase O-glycosylation and S-glutathionylation decreased in ObIR+. No evidence of differences in Tyr-nitration of catalase levels were found among groups. The study again highlights the role of erythrocytes as sensors of the inflammatory and pro-oxidant response to which these cells are subjected in children with obesity and insulin resistance.

Гепатотропні ефекти трикомпонентної противиразкової терапії та кріоекстракту плаценти: роль статевих чинників у ліпопероксидації

The purpose of the work was to reveal the role of sex factors in the processes of lipid peroxidation (LPO) against the background of chronic ethanol-tetrachloromethane-induced liver damage and the hepatotropic effects of triple antiulcer therapy and cryopreserved placenta extract (CEP). Chronic ethanol-tetrachloromethane-induced liver damage was induced by the introduction of a CCl4 solution in combination with an ethanol solution for 45 days. The content of reactants with thiobarbituric acid (TBA-active products) and catalase activity were measured in liver homogenates. Modulation of the content of sex hormones was achieved by surgical ovariectomy or testectomy. The study showed that the combined intravenous administration of esomeprazole, clarithromycin and metronidazole to rats with chronic ethanol-tetrachloromethane-induced liver damage caused an inhibition of the antioxidant defense system, this was indicated by a statistically significant decrease in catalase activity by 38.4% and a decrease in the antioxidant-prooxidant index by 35.1%, compared with the parameters of intact rats. The most significant activation of LPO processes was noted in females against the background of chronic ethanol-tetrachloromethaneinduced liver damage and the administration of anti-ulcer drugs after ovariectomy. In this case, the content of TBAactive products was 36.1 ± 2.79 μmol/kg of tissue. It was established that in castrated females, the combined use of anti-ulcer drugs and CEP against the background of chronic ethanol-tetrachloromethane-induced liver damage leveled the activation of LPO processes, this was indicated by a statistically significant (P < 0.001) 2.7 times lower content of TBA-active products in liver homogenates.

Does age pay off? Effects of three-generational experiments of nanodiamond exposure and withdrawal in wild and longevity-selected model animals.

Nanodiamonds (NDs) are considered a material with low toxicity. However, no studies describe the effects of ND withdrawal after multigenerational exposure. The aim was to evaluate ND exposure (in the 1st and 2nd generations) effects at low concentrations (0.2 or 2mgkg-1) and withdrawal (in the 3rd generation) in the wild (H) and longevity-selected (D) model insect Acheta domesticus. We measured selected oxidative stress parameters, immunity, types of cell death, and DNA damage. Most of the results obtained in the 1st generation, e.g., catalase (CAT), total antioxidant capacity (TAC), heat shock proteins (HSP70), defensins, or apoptosis level, confirmed no significant toxicity of low doses of NDs. Interestingly, strain-specific differences were observed. D-strain crickets reduced autophagy, the number of ROS+cells, and DNA damage. The effect can be a symptom of mobilization of the organism and stimulation of physiological defense mechanisms in long-living organisms. The 2nd-generation D-strain insects fed ND-spiked food at higher concentrations manifested a reduction in CAT, TAC, early apoptosis, and DNA damage, together with an increase in HSP70 and defensins. ROS+cells and cells with reduced membrane potential and autophagy did not differ significantly from the control. H-strain insects revealed a higher number of ROS+cells and cells with reduced membrane potential, decreased CAT activity, and early apoptosis. Elimination of NDs from the diet in the 3rd generation did not cause full recovery of the measured parameters. We noticed an increase in the concentration of HSP70 and defensins (H-strain) and a decrease in apoptosis (D-strain). However, the most visible increase was a significant increase in DNA damage, especially in H-strain individuals. The results suggest prolonged adverse effects of NDs on cellular functions, reaching beyond "contact time" with these particles. Unintentional and/or uncontrolled ND pollution of the environment poses a new challenge for all organisms inhabiting it, particularly during multigenerational exposure.

CORRELATIONS BETWEEN THE INDICATORS OF INFLAMMATION IN THE LIVER AND OSTEODYSTROPHIC CHANGES IN THE BONES IN RATS WITH HYPERVITAMINOSIS A

Background. The long-term therapy of dental diseases by the retinol especially in the cases of the use of high doses can lead to the significant accumulation of vitamin А in an organism, the results of which are such manifestations of the hypervitaminosis A signs as inflammation and development of liver fibrosis and activation of the destructive processes in the bones. Studying the correlation between indicators of the states of the liver and the bone system can be useful for monitoring the state of human bones through the liver indicators during long-term treatment with vitamin A, for example the dentistry diseases of different etiologies. Objective. To investigate the correlation between biochemical indicators of inflammation and antioxidant protection in the liver and the density and the composition of tubular bones and vertebrae in rats under the conditions of high-dose vitamin A use against a periodontitogenic diet. Materials and methods. Experiments were performed on male and female white Wistar rats aged 1 month. At the first stage, periodontitis was simulated with a periodontitogenic diet and the effect of this diet on the density of femur bones was determined. At the second stage, against the background of using this diet, hypervitaminosis A was simulated by introducing retinol at a dose of 8000 IU per 1kg of body weight for 56 days. The following parameters were determined: degree of atrophy of alveolar process of the jaws, density and content of the mineral (MC) and organic (OC) components of the femurs (FF) and lumbar vertebrae (LV), the activities of elastase, catalase, acid phosphatase, urease and the content of malondialdehyde (MDA) in liver tissues. Pearson’s correlation coefficients were calculated between liver and bone parameters. Results. Keeping rats on a periodontitogenic diet led to a probable increase in F density: by 11.4–12.4%. The excess intake of vitamin A caused a decrease in the density of FF by 6.4–8.8%, LV by 9.1–9.2%, a decrease in the content of MC in FF by 8.4–12.9%, in LV by 11.2–12.7%, increase of OK in FF by 3.5–7.8%, in LV by 5.2–5.5%. The formation of hypervitaminosis A in liver tissues led to an increase in elastase activity by 39.9–51.3%, acid phosphatase activity by 23.0–23.2%, urease activity by 24.7–29.8%, MDA content by 34.6%–63.7%, a decrease in catalase activity by 3.1–3.8%. The highest correlation with bone state indicators was noted for elastase activity (r > 0.8) and MDA content (r > 0.6) in liver tissues for male and female rats in general. The correlation was negative with the density and content of the mineral component, and positive with the content of the organic component. Liver catalase activity was positively correlated with bone density and mineral content (r >0.7) only in males. Liver acid phosphatase activity was negatively correlated with the density and content of the mineral component of femur bones (r > 0.6) in males. Conclusions. The hypervitaminosis A formation against the background of a periodontogenic diet leads to a decrease in bone density due to the inhibition of mineralization and the activations of bone resorption, and to inflammation and oxidative stress in liver tissues. The reliable correlation between elastase activity, MDA content in liver and the bone state indicators in male and female rats was revealed. The activities of catalase and acid phosphatase in liver were reliably correlated with the bone parameters only in males.

Carnosine and crocin ameliorate oxidative stress in rats with rhabdomyolysis-induced acute kidney injury through upregulating HO-1 gene expression

We aimed to investigate whether carnosine (a natural dipeptide found in humans) and crocin (a natural product extracted from saffron and gardenia) can prevent the harmful effects of acute kidney injury (AKI) caused by glycerol-induced rhabdomyolysis with a focus on the role of the nuclear factor E2-related factor-2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway. Thirty-six male Wistar rats were divided into 6 groups: 3 of them received saline, carnosine, and crocin IP for 7 days and the other 3 groups received the same treatment in addition to a single IM injection of 50% glycerol (10 ml/kg, divided between the two limb muscles) on 8th day. All animals were sacrificed after 24 h of the IM injection. Blood samples, muscles, and kidneys were collected for further investigations. Rhabdomyolysis was evidenced by the histopathological alterations in muscle sections and increased levels of myoglobin in kidney tissue homogenate samples. Kidney injury was characterized by increased creatinine, kidney injury molecule-1, malondialdehyde, nitric oxide, and decreased catalase activity. The injury also increased inflammatory markers and histopathological alterations in kidney sections. All these effects were corrected by pretreatment with carnosine and crocin. Both agents could also elevate HO-1 gene expression. However, both agents failed to restore the declined Nrf2 expression in glycerol-treated groups. Carnosine and crocin can effectively prevent rhabdomyolysis-induced AKI in rats through augmenting gene expression of HO-1 and antioxidant system and suppressing the generation of reactive oxygen species, lipid peroxidation, and inflammatory response.

Інтенсивність вільнорадикальних процесів у скелетних м’язах щурів за умов різної забезпеченості раціону нутрієнтами

The intensity of free-radical processes in the skeletal muscles of rats at different dietary supply with protein and sucrose was studied. It has been established that the most pronounced intensification of free radical processes in the mitochondria of skeletal muscles is found in animals kept on a low-protein/ high-sucrose diet. In particular, the generation of superoxide anion-radical increases more than 5,3-fold and the generation of hydroxyl radical more than 3,2-fold compared with the control, more than a 14,3-fold increase in the carbonyl derivatives levels, and also decreases by three times in the free protein SH-groups levels against the background of a 1,7-fold decrease in catalase activity. It has been shown that excessive consumption of sucrose is a critical factor influencing the intensity of free radical processes in skeletal muscle mitochondria. The detected changes can be considered as prerequisites for skeletal muscle dysfunction under the conditions of nutrient imbalance.

Apocynin loaded silver nanoparticles displays potent in vitro biological activities and mitigates pyrogallol-induced hepatotoxicity

Drug-loaded nanoparticles are currently gaining attention due to their improved drug delivery properties. Apocynin, a natural polyphenolic compound, is a component of many plants. It has many medicinal and pharmacological properties. Pyrogallol is an anti-psoriatic agent. However, its clinical usage is limited due to its cumulative and dose-dependent hepatotoxicity. The objective of this study was to synthesize silver nanoparticles coated with Apocynin (Apo-AgNPs), and investigate the antioxidant and liver protective effects of Apo-AgNPs on pyrogallol-induced toxicity in rats. The nanoparticles were characterized and it was determined that the synthesis technique results in homogeneously dispersed core–shell Ag structures with spherical forms and an average diameter of 13 nm (6.3 nm). Our results showed that Apo-AgNPs exhibited potent antioxidant and excellent membrane stability activities in vitro. In rats, Apo-AgNPs (10 and 30 mg/kg) significantly prevented pyrogallol-induced elevations of alkaline phosphatase, gamma-glutamyl transferase, creatinine, urea, aspartate aminotransferase, alkaline aminotransferase, total bilirubin, and decreased blood levels of uric acid. Moreover, Apo-AgNPs restored the decreased activities of the liver antioxidant enzymes, including superoxide dismutase and glutathione peroxidase, glutathione transferase, as well as non-enzyme antioxidant glutathione, as well as significantly decreased catalase activities which were induced by pyrogallol treatment. Histological studies indicated that pyrogallol -induced liver damage was alleviated following Apo-AgNPs treatment in rats. Apo-AgNPs significantly suppressed the up-regulation of Cyclooxygenase-2 (COX-2), Interleukin 6 (IL-6) and Nuclear factor-κB (NF-κB) protein expression. These results indicated that Apo-AgNPs protected the rats from damage via preserving the antioxidant defense systems, lowering pro-inflammatory cytokines, and expression of COX-2 and NF-κB in rats.

Using carbon dioxide-added microalgal-bacterial granular sludge for carbon-neutral municipal wastewater treatment under outdoor conditions: Performance, granule characteristics and environmental sustainability

Microalgal-bacterial granular sludge (MBGS) process has a gorgeous prospect for municipal wastewater treatment, but the research on the treatment of complex organic wastewater by MBGS process with CO2 addition under outdoor conditions is not enough. Therefore, this paper evaluated the feasibility of CO2-added MBGS process for complex organic wastewater disposal under natural day-night cycles. The results showed that the addition of CO2 overall improved the removal efficiency of pollutants. Typically, the removal efficiency of total phosphorus increased averagely from 88.5 % to 95.0 % in 12-h day cycle and from 26.2 % to 45.3 % in 12-h night cycle. The addition of CO2 increased the size of MBGS from 1.0 mm to 16.5 mm within 30 days due to extracellular polymeric substances secretion and the dominant filamentous microalgae on granules. The decrease of catalase activity and malondialdehyde content indicated that CO2 reduced oxidative damage and maintained the normal growth of MBGS. Further estimates of the collected gas showed that CO2-added MBGS process could reduce global CO2 emissions by one hundred million tons per year. This study is expected to contribute to the goal of carbon neutrality in the area of wastewater treatment by MBGS process.

ANTI-LITHIATIC EFFECT OF LYCOPENE IN CHEMICALLY INDUCED NEPHROLITHIASIS IN RATS

Objective: The search for anti-calculi drugs from natural sources has been believed of greater importance. Hence, the present study explored the effectiveness of lycopene against experimentally induced nephrolithiasis. Methods: The experimental study lasted for 28 days. Adult male Wistar rats were divided into six groups. Group I (Normal control) received drinking water. Group II (Disease control) received 0.75% ethylene glycol and 1% ammonium chloride in drinking water to induce nephrolithiasis. Group III–V was treated with lycopene (50 mg/kg, 100 mg/kg, and 200 mg/kg, p.o.) along with 0.75% ethylene glycol and 1% ammonium chloride. Group VI treated standard (750 mg/kg, p.o.) along with 0.75% ethylene glycol and 1% ammonium chloride. Results: The study results showed significantly high levels of urinary and serum creatinine, urea, calcium, and uric acid levels and a decrease in magnesium levels in Group II (Disease control) compared with Group I (Normal control). Treatment with lycopene (50 mg/kg, 100 mg/kg, and 200 mg/kg) restored the elevated urinary and serum parameters in Group III–VI compared with Group II. Ethylene glycol administrations lead to the production of oxidative stress and decrease superoxide dismutase, reduced glutathione, and catalase activity. Lycopene treatment restored the elevated oxidative stress parameters to normal. Histologically, lycopene has alleviated the damaged integrity of the renal structure. Conclusion: Supplementation with lycopene (100 mg/kg and 200 mg/kg) reduces and prevents the toxicity caused by ethylene glycol administration and protects the renal cells from damage.

Effect of Selenium on the Iron Homeostasis and Oxidative Damage in Brain and Liver of Mice.

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.