Stimulated Lipid Peroxidation Research Articles

THE CONTENT OF PROSTANOIDS AND CYCLOOXYGENASES IN COLON TISSUE IN EXPERIMENTAL ULCERATIVE COLITIS

Introduction. The article examines changes in the content of prostaglandins and cyclooxygenases (COX) in colon tissue in ulcerative colitis induced by 2,4-dinitrobenzene sulfonic acid (DNBS) in a 50% ethanol solution. Based on the obtained results, the authors conclude that changes in the content of the studied parameters, except PGI2, are due to ethanol effect, not DNBS. Both COX isozymes are expressed in normal colon and reduced in ulcerative colitis.
 The aim. To study the prostanoids (PGE2, PGI2, PGF2α, TBX2 and 8-iso-PGF2α) and COX-1 and -2 contents in colon tissue in experimental ulcerative colitis.
 Materials and methods. The determination of prostanoids and cyclooxygenases contents in colon tissue by enzyme immunosorbent assay was carried out on three groups of sexually mature laboratory rats of both sexes of the WAG population (1st control group – intrarectal injection of saline; 2nd control group – injection of 50% ethanol; experimental group – injection of DNBS in 50% ethanol).
 Results. PGE2 and PGI2 contents in colon tissue of experimental group rats were statistically significantly higher compared 1st and 2nd control groups. The content of PGE2 was also increased in 2nd control group versus 1st control one. The increasing PGI2 in 2nd control group versus 1st control was not significant. TBX2 and PGF2α contents in experimental and 2nd control groups were significantly lower compared 1st control. 8-iso-PGF2α (non-enzymatically derived prostanoid) level in experimental group rats was significantly higher compared both controls. 8-iso-PGF2α content in 2nd control group was significantly higher compared 1st one. The content of both COX isoforms in colon tissue in experimental group and 2nd control group rats was significantly lower compared to 1st control group.
 Conclusions. Both isoforms of COX are expressed in control group colon indicating COX-2 involvement in supporting physiological functions of normal colon tissue. All studied indicators changes, except PGI2, are due to ethanol, not DNBS. Both 50% ethanol and DNBS in 50% ethanol stimulate lipid peroxidation, confirmed by significant increase in 8-iso-PGF2α content. PGE2 and PGF2α contents changes against the background of reduced levels of COX-1 and COX-2 in experimental ulcerative colitis are most likely an adaptive response aimed at maintaining colon homeostasis. PGI2 content changes are due to DNBS, and not to ethanol.

PTC596-Induced BMI-1 Inhibition Fights Neuroblastoma Multidrug Resistance by Inducing Ferroptosis.

Neuroblastoma (NB) is a paediatric cancer with noteworthy heterogeneity ranging from spontaneous regression to high-risk forms that are characterised by cancer relapse and the acquisition of drug resistance. The most-used anticancer drugs exert their cytotoxic effect by inducing oxidative stress, and long-term therapy has been demonstrated to cause chemoresistance by enhancing the antioxidant response of NB cells. Taking advantage of an in vitro model of multidrug-resistant (MDR) NB cells, characterised by high levels of glutathione (GSH), the overexpression of the oncoprotein BMI-1, and the presence of a mutant P53 protein, we investigated a new potential strategy to fight chemoresistance. Our results show that PTC596, an inhibitor of BMI-1, exerted a high cytotoxic effect on MDR NB cells, while PRIMA-1MET, a compound able to reactivate mutant P53, had no effect on the viability of MDR cells. Furthermore, both PTC596 and PRIMA-1MET markedly reduced the expression of epithelial-mesenchymal transition proteins and limited the clonogenic potential and the cancer stemness of MDR cells. Of particular interest is the observation that PTC596, alone or in combination with PRIMA-1MET and etoposide, significantly reduced GSH levels, increased peroxide production, stimulated lipid peroxidation, and induced ferroptosis. Therefore, these findings suggest that PTC596, by inhibiting BMI-1 and triggering ferroptosis, could be a promising approach to fight chemoresistance.

High-fat high-fructose diet and alpha-ketoglutarate affect mouse behavior that is accompanied by changes in oxidative stress response and energy metabolism in the cerebral cortex

BackgroundHigh caloric diets with high amounts of fats and sweeteners such as fructose may predispose organisms to neurodegenerative diseases. MethodsThis study aimed to examine the effects of a high-fat high-fructose diet (HFFD) on the behavior of mice, energy metabolism, and markers of oxidative stress in murine cerebral cortex. Dietary α-ketoglutarate (AKG) was chosen as a treatment which could modulate the putative effects of HFFD. ResultsWe found that HFFD stimulated locomotion and defecation in mice, whereas an AKG-supplemented diet had a proclivity to promote anxiety-like behavior. HFFD stimulated lipid peroxidation, and in turn, the AKG-supplemented diet led to a higher ratio of reduced to oxidized glutathione, higher activity of NAD(P)H:quinone oxidoreductase 1, and higher mRNA levels of UDP-glucose 6-dehydrogenase and transcription factor EB. Both diets separately, but not in combination, led to a decrease in the activities of glutathione peroxidase, glutathione S-transferase, and phosphofructokinase. All experimental diets resulted in lower levels of transcripts of genes encoding pyruvate dehydrogenase kinase 4 (PDK4), glycine N-methyl transferase, and peroxisome proliferator receptor γ co-activator 1. ConclusionsOur results show that diet supplemented with AKG resulted in effects similar to those of HFFD on the cerebral cortex, but elicited substantial differences between these two diets with respect to behavior, glutathione-dependent detoxification, and processes related to autophagy. General significanceOur study provides insight into the metabolic effects of HFFD alone and in combination with alpha-ketoglutarate in the mouse brain.

Mitochondrial Lipid Peroxidation Is Responsible for Ferroptosis.

Ferroptosis induced by erastin (an inhibitor of cystine transport) and butionine sulfoximine (an inhibitor of glutathione biosynthesis) was prevented by the mitochondria-targeted antioxidants SkQ1 and MitoTEMPO. These effects correlate with the prevention of mitochondrial lipid peroxidation, which precedes cell death. Methylene blue, a redox agent that inhibits the production of reactive oxygen species (ROS) in complex I of the mitochondrial electron transport chain, also inhibits ferroptosis and mitochondrial lipid peroxidation. Activation of ROS production in complex I with rotenone in the presence of ferrous iron stimulates lipid peroxidation in isolated mitochondria, while ROS produced by complex III are ineffective. SkQ1 and methylene blue inhibit lipid peroxidation. We suggest that ROS formed in complex I promote mitochondrial lipid peroxidation and ferroptosis.

Mass Spectrometry Analysis of DNA and Protein Adducts as Biomarkers in Human Exposure to Cigarette Smoking: Acrolein as an Example.

Acrolein is a major component in cigarette smoke and a product of endogenous lipid peroxidation. It is difficult to distinguish human exposure to acrolein from exogenous sources versus endogenous causes, as components in cigarette smoke can stimulate lipid peroxidation in vivo. Therefore, analysis of acrolein-induced DNA and protein adducts by the highly accurate, sensitive, and specific mass spectrometry-based methods is vital to estimate the degree of damage by this IARC Group 2A carcinogen. This Perspective reviews the analyses of acrolein-induced DNA and protein adducts in humans by mass spectrometry focusing on samples accessible for biomonitoring, including DNA from leukocytes and oral cells and abundant proteins from blood, i.e., hemoglobin and serum albumin.

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.

Neurofilament Light Chain (NF-L) Stimulates Lipid Peroxidation to Neuronal Membrane through Microglia-Derived Ferritin Heavy Chain (FTH) Secretion.

A part of the axonal cytoskeleton protein complex, neurofilament light chain (NF-L) has been suggested as a pathological hallmark in various neurological disorders, including hemorrhagic stroke, vascular dementia, and cerebral small vessel disease. Neuroaxonal debris are mainly engulfed and phagocytosed by microglia, while the effects of NF-L on microglia have not been elucidated. Ferritin heavy chain (FTH) not only reflects the age-related status of microglia but may also be secreted into the extracellular space. After treatment of microglia with varying concentrations of NF-L (0-3 μg/ml), we found robust increases in the number of secretory FTH-containing exosomes in the medium. Induction of the FTH-containing exosomes secreted from microglia stimulates neuronal loss and membrane lipid peroxidation, as assessed by CKK8 and C11-Bodipy581/591, respectively. However, this oxidative stress damage was attenuated by blocking Fth1 expression. Our results suggest that NF-L, as a biomarker of axonal injury itself, could participate in neuronal ferroptosis in a nonclassical manner by secreting FTH-containing exosomes from microglia into the extracellular matrix.

Different frying processes stimulate lipid peroxidation and promote changes in the composition of cholesterol, free fatty acids and triglycerides in the commercial clam’s tissues Venerupis decussata

Abstract This investigation was aimed to assess and evaluate the effect of frying process with three different oils (corn, olive and margarine) on fatty acids and lipid classes’ composition of clam and their impact on the nutritional value and tissues quality. The results indicated that the contents of saturated, monounsaturated and polyunsaturated fatty acids varied significantly in fried clams and frying oil. Our data demonstrated that all lipid classes’ contents increased significantly after all frying processes. It was concluded that the frying process decreased the n-3/n-6 and DHA+EPA and increased the levels of atherogenic; thrombogenic indices. Additionally, these culinary processes promoted lipid peroxidation through the enhancement of TBARs, PV and FFA. These changes were more significant and intensive after frying with margarine and corn oils followed by virgin olive oil. These results suggest that clam fried with olive oil can be classified as highly nutritive in regard to its lipid content, major fatty acid profile; and nutritional value.

Species-specific ammonia tolerance in the marine rotifers Brachionus plicatilis and Brachionus rotundiformis: Reproductive characteristics and its mechanisms

High unionized ammonia (NH3−N) is a major stress factor for rearing aquatic animals that can collapse the mass culture of rotifers in aquaculture facilities. In rotifer mass culture, concentrations of NH3-N are elevated when reaching maximum density. As NH3-N toxicity has temperature-dependent characteristics, tropical and temperate rotifers should be subjected to different levels of habitat-resource NH3-N, which could affect their physiological adaptations. To investigate the NH3-N tolerance of rotifers associated with reproductive adaptations to different habitats, two rotifer species in the Brachionus plicatilis species complex were studied: temperate B. plicatilis and tropical B. rotundiformis. Survival, life history parameters, and reproductive patterns were assessed under acute (lethal) and chronic (sub-lethal) NH3-N exposure. These rotifer species were not treated with NH3-N or exposed to 1.1 and 8.5 mg/L NH3-N for 7 days to define the biochemical (i.e., oxidative and lipid metabolism) and behavioral (swimming speed) mechanisms of ammonia species sensitivity. High concentrations of NH3-N (≥8.5 mg/L) suppressed rotifer growth and reproduction, resulting in substantial maturation retardation and fecundity reduction in both species. Nevertheless, the tropical B. rotundiformis was more tolerant to acute and chronic NH3-N exposure than the temperate B. plicatilis, with 1.5 and 1.7 fold higher LC50 and EC50 (for intrinsic growth rate) values at 25 °C, respectively. Furthermore, B. rotundiformis showed stronger ammonia tolerance in sexual reproductive parameters, including mixis, fertilization, and resting egg production. High sexual reproduction tolerance is important for improving rotifer stress resistance and maintaining the population under harsh environments. The two species exhibited different modulations of lipid and stress defense activities under NH3-N exposure. Temperate B. plicatilis showed reduced neutral lipid accumulation in the reproductive organs (vitellarium/ovary), stimulated lipid peroxidation with a high level of malondialdehyde (MDA), and disrupted antioxidant activities. In contrast, the tropical B. rotundiformis exhibited active defense responses, with enhanced antioxidant activity and lipid synthesis. These findings with molecular evidence indicate the specific ammonia sensitivity between tropical and temperate rotifers, and more active anti-stress strategies of the tropical species than the temperate species, contributing to high ammonia tolerance. The higher ammonia tolerance of tropical B. rotundiformis species may support their high-density endurance during mass culture.

PKCα Inhibition as a Strategy to Sensitize Neuroblastoma Stem Cells to Etoposide by Stimulating Ferroptosis.

Cancer stem cells (CSCs) are a limited cell population inside a tumor bulk characterized by high levels of glutathione (GSH), the most important antioxidant thiol of which cysteine is the limiting amino acid for GSH biosynthesis. In fact, CSCs over-express xCT, a cystine transporter stabilized on cell membrane through interaction with CD44, a stemness marker whose expression is modulated by protein kinase Cα (PKCα). Since many chemotherapeutic drugs, such as Etoposide, exert their cytotoxic action by increasing reactive oxygen species (ROS) production, the presence of high antioxidant defenses confers to CSCs a crucial role in chemoresistance. In this study, Etoposide-sensitive and -resistant neuroblastoma CSCs were chronically treated with Etoposide, given alone or in combination with Sulfasalazine (SSZ) or with an inhibitor of PKCα (C2-4), which target xCT directly or indirectly, respectively. Both combined approaches are able to sensitize CSCs to Etoposide by decreasing intracellular GSH levels, inducing a metabolic switch from OXPHOS to aerobic glycolysis, down-regulating glutathione-peroxidase-4 activity and stimulating lipid peroxidation, thus leading to ferroptosis. Our results suggest, for the first time, that PKCα inhibition inducing ferroptosis might be a useful strategy with which to fight CSC chemoresistance.

Redox Modulation and Induction of Ferroptosis as a New Therapeutic Strategy in Hepatocellular Carcinoma

Ferroptosis, a newly discovered form of cell death mediated by reactive oxygen species (ROS) and lipid peroxidation, has recently been shown to have an impact on various cancer types; however, so far there are only few studies about its role in hepatocellular carcinoma (HCC). The delicate equilibrium of ROS in cancer cells has found to be crucial for cell survival, thus increased levels may trigger ferroptosis in HCC.In our study, we investigated the effect of different ROS modulators and ferroptosis inducers on a human HCC cell line and a human hepatoblastoma cell line. We identified a novel synergistic cell death induction by the combination of Auranofin and buthionine sulfoxime (BSO) or by Erastin and BSO at subtoxic concentrations. We found a caspase-independent, redox-regulated cell death, which could be rescued by different inhibitors of ferroptosis. Both cotreatments stimulated lipid peroxidation. All these findings indicated ferroptotic cell death. Both cotreatments affected the canonical ferroptosis pathway through GPX4 downregulation. We also found an accumulation of Nrf2 and HO-1, indicating an additional effect on the non-canonical pathway. Our results implicate that targeting these two main ferroptotic pathways simultaneously can overcome chemotherapy resistance in HCC.

The effect of cadmium loading on the activity of the enzyme link of the glutathione system of bull organism

One of the ultimate manifestations of Cadmium's toxic effects is the depletion of the animal's antioxidant protection system. The article presents data on the effect of cadmium chloride at a dose of 0.04 mg/kg body weight on the activity of enzymes of the glutathione system of antioxidant protection of the body of young cattle. The surveys were conducted on the basis of farm Ivanivtsi of Zhydachiv district of Lviv region on 10 bulls of six months old, Ukrainian black-ruffed dairy breed, which were formed into 2 groups of 5 animals each: control and experimental. Bulls of the experimental group were fed with feed cadmium chloride at a dose of 0.04 mg/kg body weight of the animal. For research, the rules were compulsory for performing zootechnical experiments on the selection and retention of analogues in groups, technology for the procurement, use and accounting of feed consumed. The diet of the animals was balanced by the nutrients and minerals that provided for their need for essential nutrients. The results of studies indicate that Cadmium significantly affects the metabolism processes in liver cells, and thus stimulates lipid peroxidation processes and inhibits the activity of enzymes of the glutathione link of the antioxidant system. The lowest activity of the enzyme link of the glutathione system of antioxidant protection of the body of cattle was found on the twentieth day of the experiment, where, accordingly, the activity of glutathione peroxidase in the serum of bugs of the experimental group decreased by 22.6%, the activity of glutathione 6 phosphate dehydrogenase – by 24.3% relative to the control group of animals. The inhibition of the activity of enzymes of the glutathione system of the organism of bulls of the experimental group is caused by the development of oxidative stress caused by the feeding of Cadmium. The researches made it possible to reveal more deeply the pathogenesis of the toxic effect of cadmium on the body of bugs and use these data in the development of an antidote for cadmium intoxication.

Effects of Vitamins C and E on Free Radical Processes in the Blood of Rats in Acute Moderate Hypothermia

We assessed the effect of intraperitoneal administration of ascorbic acid (vitamin C, 100 mg/kg/day) and α-tocopherol (vitamin E–selenium, 40 mg/kg/day), given alone or in combination for seven days, on the intensity of free-radical processes in the blood of rats in acute short-term hypothermia of 30○С. Hypothermia contributes to the development of oxidative stress in erythrocytes, stimulating the lipid peroxidation and oxidative modification of proteins (OMP), decreasing the content of glutathione (GSH) and increasing the activity of superoxide dismutase (SOD) in erythrocytes. A separate administration of vitamins prevents a decrease in the level of GSH and an increase in the activity of SOD in erythrocytes in hypothermia, but vitamin C stimulates lipid peroxidation and OMP and vitamin E stimulates OMP of the erythrocyte membranes. Coadministration of vitamins C and E completely prevents the development of oxidative stress in erythrocytes during hypothermia.

Кластерний аналіз впливу флуренізиду на показники стану прооксидантно-антиоксидантної системи зародків в’юна

Experiments were carried out on embryos of Misgurnus fossilis L. After washing zygotes were incubated in physiological Golferre solution, containing a solution of flurenizide in concentrations of 0.01; 0.05; 0.15; 1; 5; 15 mM. The embryos were harvested for 60, 150, 210, and 330 minutes after fertilization of the 1 st (2 blastomeres), 4 th (16 blastomeres), 6 th (64 blastomeres), 8 th (256 blastomeres) and 10 th (1024 blastomeres) crushing egg zygotes. The intensity of lipids peroxide oxidation processes was evaluated by measuring of the content of lipid hydroperoxides and TBA-reactive substances. The state of antioxidant system was studied with the activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase. Cluster analysis was conducted to identify stages of development that have the same changes of the content of lipid hydroperoxides, TBА-reactive substances, activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase. Applying a cluster analysis it was found that before the stage of 64 blastomeres, all experimental groups were divided into 4 groups of similarity according to the studied indicators. Flurenizide in concentration of 0.05 mM in stage of 2 blastomers was found to have no significant effect on values whose were at the control level. Fluinizide in concentrations of 5 and 15 mM results in a significant decrease (compared with control) in the content of TBА-reactive substances, increasing of content of lipid hydroperoxides and decreasing of activity of catalase, glutathione peroxidase and glutathione-S-transferase. At the stage of development of 256 and 1024 blastomeres, all groups are divided into 5 groups of similarity, indicating change in the effect of flurenizyd on these stages of loach embryos development. In particular, at the development stage of 1024 blastomeres, flurenizide in a concentration of 1 mM leads to more pronounced increase in intensity of free radical processes, as well as the decrease in activity of superoxide dimitase, catalase, glutathione peroxidase and glutathione-S-transferase. It is known that this concentration is a daily therapeutic dose for an adult. It is likely that it is harmful to the germinal cells of liver, since it stimulates lipid peroxidation and suppresses antioxidant system ensymes. It has been established that with the action of flurenizide in concentrations of 5 and 15 mM, the content of hydroperoxides increases, the activity of superoxide dimitase, glutathione peroxidase and glutathione-S-transferase decreases. However, this effect is less pronounced compared with action of flurenizide in concentration of 1 mM.

Low doses of Bisphenol A have pro-inflammatory and pro-oxidant effects, stimulate lipid peroxidation and increase the cardiotoxicity of Doxorubicin in cardiomyoblasts

Endocrine disrupters are strictly associated to cancer and several cardiovascular risk factors. Bisphenol A (BPA) is an endocrine disrupter commonly used in the manufacturing of plastics based on polycarbonate, polyvinyl chloride and resins. Our study aims to investigate whether BPA may cause pro-oxidative and pro-inflammatory effects on cardiomyoblasts, thus exacerbating the Doxorubicin (DOXO)-induced cardiotoxicity phenomena. We tested the metabolic effects of BPA at low doses analyzing its affections on the intracellular calcium uptake, oxidative stress, lipid peroxidation and production of nitric oxide and interleukins. Co-incubation of BPA and DOXO significantly reduced the cardiomyoblast viability, compared to only DOXO exposure cells. The mechanisms underlying these effects are based on the stimulation of the intracellular calcium accumulation and lipid peroxidation. Notably, BPA increase the production of pro-inflammatory interleukins involved in cardiovascular diseases as well as in DOXO-Induced cardiotoxicity phenomena. This study provides a rationale for translational studies in the field of cardio-oncology.

Nitrogen-Containing Heterocyclic Derivatives of Maleopimaric Acid by Carboxyl Function and their Antioxidant Activity

New N-heterocyclic maleopimaric acid derivatives were prepared and shown to affect free-radical oxidation in model systems, in particular, to suppress reactive oxygen species generation and stimulated lipid peroxidation in model systems containing lipoproteins.

Vitamin C Protect Against Monosodium Glutamate Mediated Oxidative Stress in the Male White Rats

The present study evaluated the ameliorative effect of vitamin C on alteration in thyroid hormones induced by monosodium glutamate. Total number of twenty male rats were divided into five groups each group contain four rats. Groups I administrated distal water and standard diet to keep as control group, group II and III were administered MSG in to two doses (8, 16g/kg) respectively. Finally, Group IV and V were administrated MSG (8, 16 g/kg with vitamin C) respectively for 30 days. The results show decrease in serum triiodothyronine, serum thyroxine, superoxide dismutase, catalase in addition significant increment in the thyroid stimulating hormone level and lipid peroxidation in the groups of rats treated with MSG only while all parameters back in to normal values in the groups of rats treated with MSG and vitamin C also, the histopathological changes appear degeneration and pyknotic cells in the thyroid gland. In conclusion, food additives as MSG have many side effects in the body when taken it for long period and vitamin C has vital role to protect the body from any foreign body.

SkQ1 Controls CASP3 Gene Expression and Caspase-3-Like Activity in the Brain of Rats under Oxidative Stress.

Here, we studied the effect of the mitochondria-targeted antioxidant SkQ1 (plastoquinone cationic derivative) on the CASP3 gene expression and caspase-3 activity in rat cerebral cortex and brain mitochondria under normal conditions and in oxidative stress induced by hyperbaric oxygenation (HBO). Under physiological conditions, SkQ1 administration (50 nmol/kg, 5 days) did not affect the CASP3 gene expression and caspase-3-like activity in the cortical cells, as well as caspase-3-like activity in brain mitochondria, but caused a moderate decrease in the content of primary products of lipid peroxidation (LPO) and an increase in the reduced glutathione (GSH) level. HBO-induced oxidative stress (0.5 MPa, 90 min) was accompanied by significant upregulation of CASP3 mRNA and caspase-3-like activity in the cerebral cortex, activation of the mitochondrial enzyme with simultaneous decrease in the GSH content, increase in the glutathione reductase activity, and stimulation of LPO. Administration of SkQ1 before the HBO session maintained the basal levels of the CASP3 gene expression and enzyme activity in the cerebral cortex cells and led to the normalization of caspase-3-like activity and redox parameters in brain mitochondria. We hypothesize that SkQ1 protects brain cells from the HBO-induced oxidative stress due to its antioxidant activity and stimulation of antiapoptotic mechanisms.

Effects of melatonin on low-dose lipopolysaccharide-induced oxidative stress in mouse liver, muscle, and kidney.

Lipopolysaccharide (LPS) administration in an in vivo experimental mice model causes oxidative damage in the liver, muscle, and kidney. We aimed to determine specific mechanisms underlying melatonin's antioxidant protective role. Assays were carried out in quadruplicate in the control, melatonin (10 mg/kg, 10 days), acute LPS administration (once 150 μg), and LPS + melatonin groups. LPS stimulated lipid peroxidation processes (dienes and malondialdehyde) and antioxidant enzyme concentrations (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) were assessed in all investigated tissues. Protein oxidation processes (measured as aldehyde and kenotic carbonyl protein derivatives) were enhanced by LPS in the kidney and liver but not in muscle. Melatonin reversed LPS-induced changes, with the exception of muscle protein oxidation. LPS-induced oxidative stress resulted in augmented early-stage diene conjugated and end-stage malondialdehyde lipid peroxidation processes and affected antioxidant activity in liver, kidney, and muscle tissues. LPS activated protein oxidation processes in the kidney and liver. Melatonin ameliorated oxidative damage in the liver, kidney, and partially in the muscle. Melatonin modulates oxidative stress-induced states. Potential synergism between melatonin and systemic inflammation in terms of oxidative modification of muscle proteins needs to be clarified in further studies.

Modulation of crude oil induced alteration of oxidative stress indices in rat by red palm oil

The toxic properties of crude oil were hitherto described. Therefore, several materials are being tested for protective potential counter to petroleum toxicity. This study evaluated the oxidative stress status of rats fed diet incorporating petroleum tainted diet with red palm oil. Four groups with six rats in each group were employed in this study. Rats in group 1 were fed with fish feed only while rats in group 2 were fed with crude oil tainted diet and rats in groups 3 and 4 were fed with contaminated feed that was pre-treated with 4 ml and 8 ml of red palm oil respectively. The rats were exposed to the respective diet for 30 days and had water freely. Thereafter standard analytical methods were used to measure oxidative stress markers in organs/tissues of rats. The results showed that crude oil tainted diet stimulated lipid peroxidation and cause decline in reduced glutathione level, superoxide dismutase and catalase activities in the organ/tissues of rats which were significant (P < 0.05) relative to control. Pre-treatment of the rat diets with red palm oil significantly (P < 0.05) drop lipid peroxidation and increase level of antioxidant markers in the organ/tissues of rats in relation to the values in rats fed with diet tainted with crude oil only. This study has confirmed that red palm oil can evade the oxidative insult elicited by crude oil intoxication in various organs/tissues. Therefore, red palm oil should be made a major dietary component for inhabitants of petroleum producing areas of the world.Keywords: Antioxidants. Diet, Palm oil, Petroleum