Measure Of Lipid Peroxidation Research Articles

SENP1 knockdown potentiates the apoptosis, cell cycle arrest, and reduces cisplatin resistance of diffuse large B cell lymphoma cells via inducing ferroptosis.

Ferroptosis has been regarded as a critical event in the process of diffuse large B cell lymphoma (DLBCL). Sentrin-specific protease 1 (SENP1) has emerged as an oncogene in multiple human malignancies. The present work was to investigate the effects of SENP1 on the progression of DLBCL and the possible regulatory mechanism involving ferroptosis. SENP1 expression in DLBCL tissues, parental and cisplatin-resistant DLBCL cells were, respectively, tested by GEPIA database, RT-qPCR, and Western blot. Cell viability was estimated via CCK-8 assay. Flow cytometry analysis estimated cell apoptosis and cycle. Western blot examined the expression of apoptosis-, cell cycle-, and ferroptosis-associated proteins. TBARS assay and BODIPY 581/591 C11 probe measured lipid peroxidation. Related assay kit assessed total iron levels. CCK-8 and flow cytometry evaluated cisplatin resistance. SENP1 expression was raised in DLBCL tissues and cells. SENP1 knockdown reduced cell viability, boosted cell apoptosis, cell cycle arrest, and elevated cisplatin sensitivity in DLBCL. SENP1 depletion drove the ferroptosis of both parental and cisplatin-resistant DLBCL cells and ferroptosis inhibitor Fer-1 reversed the influences of SENP1 inhibition on cell viability, apoptosis, cell cycle, and cisplatin resistance in DLBCL. Anyway, SENP1 absence might facilitate ferroptosis to obstruct the development of DLBCL and cisplatin resistance.

Mitochondrial Peroxiredoxin 6 Declines with Aging in Parallel with Increases in Hydrogen Peroxide Generation

Oxidative stress in cells and tissues arise from an imbalance between the generation of free radicals and the ability to detoxify these reactive oxygen species (ROS). Peroxiredoxins (PRDXs) are a family of widely distributed enzymes that act as master antioxidant regulators by scavenging peroxides and peroxynitrites. The accumulation of oxidative damage from chronic exposure to oxidative stress such as on DNA, mitochondrial proteins, and lipid macromolecules, is postulated to result in age-associated pathologies and physiological dysfunctions. Peroxiredoxin-6 (PRDX6) contributes to the maintenance of redox balance in a variety of tissues from lung to skeletal muscle. Here, we hypothesized that PRDX6 localizes to the mitochondria and plays a significant role in maintaining mitochondrial function through targeting mitochondrially generated ROS, and that gradual loss of mitochondrial PRDX6 contributes to increased oxidative stress and accumulation of oxidative damage during aging. In this study, respiratory rates and complex activities in isolated skeletal muscle mitochondria obtained from young (3-6 months) and old (20-24 months) C57/BL6J mice were compared. Amplex UltraRed fluorescence was used to determine production rates of mitochondrial hydrogen peroxide (H2O2). Western blot analysis was used to compare protein abundance and ELISA was used to measure lipid peroxidation in skeletal muscle mitochondrial fractions. Our findings revealed that isolated mitochondria from skeletal muscle in old mice generated higher rates of H2O2 from complex I (CI) during state 3 and state 4 (State 3; State 4) derived respiration (3.93 ± 0.41; 3.56 ± 0.38 pmol H2O2..s−1.mg−1) compared to young mouse mitochondria (1.57 ± 0.48; 1.89 ± 0.59 pmol H2O2.s−1.mg−1, p ≤ 0.05). This was also found when saturating amounts of ADP were used to stimulate maximal rates of oxygen consumption (old: 3.65 ± 0.77; young 1.40 ± 0.21 pmol H2O2−1.mg−1, p ≤ 0.05). Furthermore, CI activity was found to be lower in isolated mitochondria from old mice (0.65 ± 0.006 U.ug−1) compared to young mice (2.11 ± 0.64 U.ug−1, p ≤ 0.05). Similarly, mitochondrial PRDX6 abundance was lower while levels of lipid peroxidation product malondialdehyde were higher in skeletal muscle from old animals (old: 2712 ± 1320 pg.mL−1; young: 489 ± 225 pg.mL−1). These results show higher mitochondrial ROS generation rates and oxidative damage in old animals. These data also suggest that loss of PRDX6 in aging leads to mitochondrial dysfunction mediated by diminished CI activity and loss of membrane integrity. We are currently conducting mechanistic studies in cellular models with disrupted PRDX6 expression to confirm the effect of this protein in maintaining mitochondrial function. This study offers novel observations on the significance of mitochondrially localized PRDX6 in antioxidant defense as well as the sources and roles of ROS generation in contributing to an aging phenotype. National Institute of General Medical Sciences (NIGMS, Award Number R35GM146951). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Therapeutic Effects of Pimpinella anisum Fruit Extract on Polycystic Ovary Syndrome in a Rat Model: Emerging Role of Inflammatory Responses and Oxidative Stress.

Polycystic ovary syndrome (PCOS) is the most common gynecological endocrine disorder. This study evaluated the therapeutic effects of Pimpinella anisum L. (P. anisum) fruit on pro-inflammatory cytokines, oxidative stress markers, and ovarian tissue structure in a rat model of PCOS. After inducing PCOS, female Wistar rats were randomly divided into control and PCOS groups. They orally received daily doses of normal saline or hydro-alcoholic extract of P. anisum at two doses (200 and 400 mg/kg) for 21 days. At the end of the treatment period, ovarian and liver tissues were collected to measure lipid peroxidation, antioxidant status, TNF-α, IL-6 mRNA expression, and its content. Additionally, histopathological examinations of the ovarian tissue were conducted. Our findings revealed a dose-dependent change in the biochemical and histopathological parameters. Treatment with P. anisum resulted in a significant decrease in TNF-α and IL-6 mRNA expression levels and their content in the ovarian and liver tissues. It also reduced MDA levels while increasing SOD and GPx activity in both ovarian and liver tissues of PCOS rats. Furthermore, the number of follicular cysts in the PCOS rat model was significantly reduced. The beneficial effects of P. anisum in PCOS rats are partly attributed to the inhibition of inflammatory and oxidative stress markers in ovarian tissue. These findings suggest that P. anisum could be a potential candidate for the treatment of PCOS disorders.

Influence of Maternal Dietary Pattern on the Pro-Oxidant and Antioxidant Status of Mother's Own Milk.

Human milk is essential for a child's best development. However, what a mother eats while breastfeeding can directly influence the composition of mother's milk. This study aimed to assess the antioxidant-oxidant profile of human milk and establish a connection between this profile and the dietary habits of the mothers. A cross-sectional study was conducted at the Hospital Infantil e Maternidade Alzir Bernardino Alves (HIMABA), located in the municipality of Vila Velha-ES, Brazil. The sample included 98 participants. All volunteers completed a structured interview and a Food Frequency Questionnaire. Approximately 5-10 ml of colostrum, transitional milk, and mature milk were manually collected. The antioxidant activity of human milk was assessed using the colorimetric method for free radical scavenging with 2,2'-azinobis-3-ethylbenzothiazoline-6-sulfonic acid. Oxidative stress was determined by measuring lipid peroxidation through malondialdehyde concentration, evaluating advanced oxidation protein products, and assessing total protein content using the Bradford method. The antioxidant profile of colostrum was higher than that observed in later phases of milk, whereas pro-oxidants increased in later phases. Maternal dietary patterns influenced the pro-oxidant status of human milk. Participants with a higher daily intake of milk, dairy products, vegetable oils, olive oils, and legumes exhibited lower levels of lipid peroxidation in colostrum, transition milk, and mature milk, respectively. Our study highlights the vital role of a balanced maternal diet in shaping the pro-oxidant status of human milk, with implications for infant health.

Type 2 diabetes mellitus facilitates status epilepticus in adult rats: Seizure severity, neurodegeneration, and oxidative stress.

The goal of this research was to evaluate the effect of DM type 2 (DM2) on SE severity, neurodegeneration, and brain oxidative stress (OS) secondary to seizures. DM2 was induced in postnatal day (P) 3 male rat pups by injecting streptozocin (STZ) 100 mg/kg; control rats were injected with citrate buffer as vehicle. At P90, SE was induced by the lithium-pilocarpine administration and seizure latency, frequency, and severity were evaluated. Neurodegeneration was assessed 24 h after SE by Fluoro-Jade B (F-JB) staining, whereas OS was estimated by measuring lipid peroxidation and reactive oxygen species (ROS). DM2 rats showed an increase in latency to the first generalized seizure and SE onset, had a higher number and a longer duration of seizures, and displayed a larger neurodegeneration in the hippocampus (CA3, CA1, dentate gyrus, and hilus), the piriform cortex, the dorsomedial nucleus of the thalamus and the cortical amygdala. Our results also show that only SE, neither DM2 nor the combination of DM2 with SE, caused the increase in ROS and brain lipid peroxidation. DM2 causes higher seizure severity and neurodegeneration but did not exacerbate SE-induced OS under these conditions. Our research performed in animal models suggests that type 2 diabetes mellitus (DM2) may be a risk factor for causing higher seizure severity and seizure-induced neuron cell death. However, even when long-term seizures promote an imbalance between brain pro-oxidants and antioxidants, DM2 does not exacerbate that disproportion.

Evaluation of cytotoxicity impacts of combined methylene blue-mediated photodynamic therapy and intracanal antibiotic medicaments on dental stem cells

Root canal therapy is a predominant method for treatment of dental pulp and periapical diseases. Conventional methods such as mechanical instrumentations, chemical irrigation and intracanal medicaments pose a huge limitation to root canal disinfection as they kill bacteria and dental stem cells simultaneously. Therefore, much attention has been focused on finding more efficacious antibacterial methods that has no or negligible cytotoxicity for dental stem cells. Herein, we hypothesized that combining antibacterial medicaments with Antimicrobial photodynamic therapy (aPDT) and methylene blue (MB) as a photosensitizer would be effective in reducing death of dental pulp stem cells (DPSCs). To examine this, DPSCs were isolated from third molar teeth through enzymatic digestion. Isolated cells were cultured in αMEM and when reached adequate confluency, were used for further analysis. Cytotoxicity effect of different groups of MB, DAP, MB, LED and their combination on DPSCs was analyzed using MTT assay. DPSCs membrane integrity as a marker of live cells was assessed through measuring lipid peroxidation and lactate dehydrogenase (LDH) release into extracellular space. Results showed that the combination of LED, MB and TAP or aPDT, MB and DAP was more effective in reducing DPSCs death rate compared to TAP and DAP administration alone. Moreover, Malondialdehyde (MDA) and LDH levels were found to be decreased in cells exposed to combination treatment in comparison with single TAP or DAP therapy. Our study shows the promising perspectives of employing combined aPDT, MB and antibiotic medicaments for reduction of dental stem cell death.

Measuring lipid peroxidation in the presence of graphene quantum dots

Measuring lipid peroxidation in the presence of graphene quantum dots

Can pharmaceutical care decrease the oxidative stress in type 2 diabetes mellitus?

Type 2 diabetes mellitus (T2D) is a chronic metabolic disorder characterized by an increase in oxidative stress, which is itself related to development of T2D’s main chronic complications. Oxidative stress caused by elevated production of reactive species of oxygen and decrease of antioxidant defense system level, leads to activation of lipid peroxidation (LPO) and oxidative lipoprotein modification with increasing atherogenicity. Therefore, the aim of this study was to evaluate whether pharmacotherapeutic follow-up in patients with T2D, users and non-users of insulin, interferes with the levels of oxidative stress, measuring lipid peroxidation and protein oxidation, nitric oxide and superoxide dismutase levels. After the follow-up, there was a decrease in nitric oxide levels and an increase in superoxide dismutase concentration for the group with insulin therapy. Accordingly, these results show that the proposed pharmaceutical care program reduced the oxidative stress levels, mainly in patients in insulin therapy, as a consequence, can impact in the surging of the main chronic complications in T2D.

Carbon Nanodots Attenuate Lipid Peroxidation in the LDL Receptor Knockout Mouse Brain.

Abnormal cholesterol metabolism can lead to oxidative stress in the brain. Low-density lipoprotein receptor (LDLr) knockout mice are models for studying altered cholesterol metabolism and oxidative stress onset in the brain. Carbon nanodots are a new class of carbon nanomaterials that possess antioxidant properties. The goal of our study was to evaluate the effectiveness of carbon nanodots in preventing brain lipid peroxidation. LDLr knockout mice and wild-type C57BL/6J mice were treated with saline or 2.5 mg/kg bw of carbon nanodots for a 16-week period. Brains were removed and dissected into the cortex, midbrain, and striatum. We measured lipid peroxidation in the mouse brain tissues using the Thiobarbituric Acid Reactive Substances Assay and iron and copper concentrations using Graphite Furnace Atomic Absorption Spectroscopy. We focused on iron and copper due to their association with oxidative stress. Iron concentrations were significantly elevated in the midbrain and striatum of the LDLr knockout mice compared to the C57BL/6J mice, whereas lipid peroxidation was greatest in the midbrain and cortex of the LDLr knockout mice. Treatment with carbon nanodots in the LDLr knockout mice attenuated both the rise in iron and lipid peroxidation, but they had no negative effect in the C57BL/6J mice, indicating the anti-oxidative stress properties of carbon nanodots. We also assessed locomotor and anxiety-like behaviors as functional indicators of lipid peroxidation and found that treatment with carbon nanodots prevented the anxiety-like behaviors displayed by the LDLr knockout mice. Overall, our results show that carbon nanodots are safe and may be an effective nanomaterial for combating the harmful effects caused by lipid peroxidation.

Lipid stores reveal the state of the coral-algae symbiosis at the single-cell level

Coral reefs worldwide are threatened by environmental stress. The observable decline in coral cover, is principally due to the intensifying breakdown of the coral symbiosis, a process known as ‘bleaching’. Overproduction of reactive oxygen species (ROS) is considered a key driver of coral bleaching, where environmental stress leads to increased ROS expression. To explore the link between ROS damage and symbiont status, we measured lipid peroxidation (LPO), a ubiquitous form of ROS damage, in the lipid stores of individual endo- and ex-symbiotic algal cells of three coral species, using confocal microscopy and a lipid hydroperoxide sensitive fluorescent dye. We found LPO was higher in endosymbionts, while lipid volume was greater in ex-symbiotic cells. Cluster analysis revealed three metabolic profiles differentiating endosymbiotic (#1: high LPO, low lipid) and ex-symbiotic cells (#3: low LPO, high lipid), with the intermediate group (#2) containing both cell types. Heat stress caused endosymbionts of Pocillopora acuta to shift away from cluster #1, suggesting this cluster represents cells in healthy/stable symbiosis. Our study delivers a new means to assess the coral symbiosis, demonstrating that symbiont LPO ratio combined with lipid store volume is a robust metabolic marker for the state of the symbiosis at the cellular level.

A selective toxicity of Pt-coated Au nanoparticles in cancerous MCF-7 cells over non-cancerous HUVE cells

ObjectivesNitric oxide (NO) and NO-generated reactive nitrogen species (RNS) in conjunction with reactive oxygen species (ROS) have received attention for their potential in oxidative stress-based cancer therapy. Here, we report commercially obtained Pt-coated Au nanoparticles (Pt-Au NPs; 27 ± 20 nm) higher uptake and cytotoxicity in human breast cancer MCF-7 cells as compared to a non-cancerous human cell (HUVE). MethodsCytotoxicity was evaluated by MTT bioassay followed by measurement of ROS (by DCFH-DA probe) and NO (by DAR-2 probe) in live cells. Membrane integrity was evaluated by measuring lipid peroxidation by live cell dye BODIPY fluorescence, TBARS absorbance, and LDH release. Ubiquitous antioxidant GSH was also measured followed by changes in MMP status by live cell dye JC-1. Mode of cell death was determined by triple staining (Hoechst/annexin V/PI triple staining), and caspase 9 and 3 activities in cancerous MCF-7 and non-cancerous HUVE cell lines. ResultsMCF-7 cells exhibited a 63 ± 5 % higher tendency of Pt-Au NPs uptake in comparison to HUVE cells. Accordingly, IC50 of Pt-Au NPs came out to be 0.48 ± 0.09 µM in MCF-7 cells and 0.93 ± 0.11 µM in non-cancerous HUVE cells. Therefore, the cytotoxic potential of NPs in MCF-7 cells was almost 1.9-fold higher than in HUVE cells indicating cancer cells are significantly more susceptible to death than HUVE cells with a normal tissue origin. NPs caused a significant induction in oxidative stress and loss in MMP in the two cells. ConclusionWe realize two major facts from this study that goes in the favor of anticancer potential of Pt-Au NPs. The first reason is the high internalization of NPs in MCF-7 cells as compared to that in HUVE cells. The second reason is that HUVE cells were found not as expressive for NO as were MCF-7 cells.

Oxidative stress and PON1 (T172A/L55M) polymorphism: potential risk factors for Osteoarthritis

Objective: To investigate the role of oxidative stress in the progression of osteoarthritis with the genetic determinant of paraoxonase-1 enzyme L55M in osteoarthritis patients. Method: The case control study was carried out at the University of Karachi from April to November 2020, and comprised blood samples of female osteoarthritis patients aged >50 years and healthy controls matched for age and gender. Oxidative stress was assessed by measuring lipid peroxidation product and protein carbonyl content. Activities of paraoxonase-1 paraoxonase and arylesterase were evaluated in the subjects. Protein expression of paraoxonase-1 was also analysed using western blot method. Paraoxonase-1 L55M (rs854560) polymorphism was determined using tetra-amplification-refractory mutation system polymerase chain reaction. Data was analysed using SPSS® Statistics 20.0. Results: Of the 103 subjects, 50(48.5%) were patients and 53(51.5%) were controls. The overall age range was 50-70 years. The extent of malondialdehyde (p<0.001) and protein carbonyl content (p<0.05) were increased significantly in the patients compared to the controls. Activity of paraoxonase and arylesterase was found decreased (p<0.001) in patients compared to the controls. The prevalence of genotype MM was higher in the patients than the controls(p=0.001). L55M was more pronounced in patients suffering than the controls (p=0.01). Conclusion: The elevated levels of malondialdehyde and cabonylated protein content might be associated with osteoarthritis progression. Decreased serum paraoxonase-1 activity with L55M was the major consequence of oxidative stress in female osteoarthritis patients. Key Words: Osteoarthritis, Oxidative stress, Paraoxonase, Polymorphism.

Chlorpyrifos stimulates ABCC-mediated transport in the intestine of the rainbow trout Oncorhynchus mykiss

The organophosphorus pesticide chlorpyrifos, detected in water and food worldwide, has also been found in the Río Negro and Neuquén Valley, North Patagonia, Argentina, where the rainbow trout, Oncorhynchus mykiss, is one of the most abundant fish species. We analyzed whether chlorpyrifos affects the transport activity of the ATP-binding cassette protein transporters from the subfamily C (ABCC), which are critical components of multixenobiotic resistance.We exposed ex vivo O. mykiss middle intestine strips (non-polarized) and segments (polarized) for one hour to 0 (solvent control), 3, 10, and 20 μg L−1 and to 0, 10, and 20 μg L−1 chlorpyrifos, respectively. We estimated the Abcc-mediated transport rate by measuring the transport rate of the specific Abcc substrate 2,4-dinitrophenyl-S-glutathione (DNP-SG). In addition, we measured the enzymatic activity of cholinesterase, carboxylesterase, glutathione-S-transferase, and 7-ethoxyresorufin-O-deethylase (EROD, indicative of the activity of cytochrome P450 monooxygenase 1A, CYP1A). We also measured lipid peroxidation using the thiobarbituric acid reactive substances method and the gene expression of Abcc2 and genes of the AhR pathway, AhR, ARNT, and cyp1a, by qRT-PCR. Chlorpyrifos induced the DNP-SG transport rate in middle intestine strips in a concentration-dependent manner (49–71%). In polarized preparations, the induction of the DNP-SG transport rate was observed only in everted segments exposed to 20 μg L−1 chlorpyrifos (40%), indicating that CPF only stimulated the apical (luminal) transport flux. Exposure to chlorpyrifos increased GST activity by 42% in intestine strips and inhibited EROD activity (47.5%). In addition, chlorpyrifos exposure inhibited cholinesterase (34–55%) and carboxylesterase (33–42.5%) activities at all the concentrations assayed and increased TBARS levels in a concentration-dependent manner (71–123%). Exposure to 20 μgL−1 chlorpyrifos did not affect the mRNA expression of the studied genes. The lack of inhibition of DNP-SG transport suggests that chlorpyrifos is not an Abcc substrate. Instead, CPF induces the activity of Abcc proteins in the apical membrane of enterocytes, likely through a post-translational pathway.

Mitochondrial respiration in thoracic perivascular adipose tissue of diabetic mice

Thoracic perivascular adipose tissue (tPVAT) has a phenotype resembling brown AT. Dysfunctional tPVAT appears to be linked to vascular dysfunction. We evaluated uncoupling protein 1 (UCP1) expression by Western blot, oxidative stress by measuring lipid peroxidation, the antioxidant capacity by HPLC and spectrophotometry, and mitochondrial respiration by high-resolution respirometry (HRR) in tPVAT, compared to inguinal white AT (iWAT), obtained from non-diabetic (NDM) and streptozocin-induced diabetic (STZ-DM) mice. Mitochondrial respiration was assessed by HRR using protocol 1: complex I and II oxidative phosphorylation (OXPHOS) and protocol 2: fatty acid oxidation (FAO) OXPHOS. OXPHOS capacity in tPVAT was also evaluated after UCP1 inhibition by guanosine 5'-diphosphate (GDP). UCP1 expression was higher in tPVAT when compared with iWAT in both NDM and STZ-DM mice. The malondialdehyde concentration was elevated in tPVAT from STZ-DM compared to NDM mice. Glutathione peroxidase and reductase activities, as well as reduced glutathione levels, were not different between tPVAT from NDM and STZ-DM mice but were lower compared to iWAT of STZ-DM mice. OXPHOS capacity of tPVAT was significantly decreased after UCP1 inhibition by GDP in protocol 1. While there were no differences in the OXPHOS capacity between NDM and STZ-DM mice in protocol 1, it was increased in STZ-DM compared to NDM mice in protocol 2. Moreover, complex II- and FAO-linked respiration were elevated in STZ-DM mice under UCP1 inhibition. Pharmacological therapies could be targeted to modulate UCP1 activity with a significant impact in the uncoupling of mitochondrial bioenergetics in tPVAT.

Quality of dietary carbohydrate is more important than its quantity in lipid peroxidation

High glycemic index (GI) diets have been linked to elevated risk of cardiometabolic diseases. One possible underlying mechanism comes from high GI diet's potential to promote lipid peroxidation. We aim to evaluate whether and to what extent dietary carbohydrate quality and quantity are associated with systemic levels of lipid peroxidation in females. In this cross-sectional analysis of 2163 middle-aged women, a subset of the Shanghai Women's Health Study, we measured lipid peroxidation biomarkers F2-isoprostanes (F2-IsoPs) and its metabolite, 2,3-dinor-5,6-dihydro-15-F2t-IsoP (F2-IsoP-M), in urine. The quality of carbohydrate was defined by dietary GI, assessed using a validated FFQ via in-person interviews. A multivariable linear regression model with restricted cubic spline functions was used to evaluate the association of measured biomarkers with carbohydrate intake and dietary GI. After adjustment for potential confounding factors such as cigarette smoking, BMI, and comorbidities, among others, we found that F2-IsoP-M concentrations were positively associated with both carbohydrate intake and dietary GI. Carbohydrate intake and dietary GI were weakly correlated (r=0.12). When further mutually adjusted for the 2 factors, the positive association with F2-IsoP-M remained statistically significant for GI (P=0.004) but not for carbohydrate intake (P=0.50). Compared with those in the 10th percentile of dietary GI, fold increases (95% CI) in F2-IsoP-M concentrations for those in the 30th, 50th, 70th, and 90th percentiles were 1.03 (1.00, 1.07), 1.06 (1.01, 1.10), 1.09 (1.03, 1.14), and 1.13 (1.05, 1.21), respectively. Moreover, there appeared a threshold regarding the association between dietary GI and F2-IsoP-M concentrations, with the dose-effect slope of GI being 2.3 times greater when GI was≥75 relative to GI<75. This study provides evidence that the quality of dietary carbohydrate may be more important than the quantity of the intake with regard to systemic lipid peroxidation.

Comparative study on the oxidative stress of commercially important fish species from localities with different ecological conditions along the Bulgarian Black Sea coast

The aim of the present study was to perform a pilot assessment and analysis of the oxidative stress (OS) level in four commercially important fish species (round goby, red mullet, sprat and horse mackerel) from different localities of the Bulgarian Black Sea coast. The fish were sampled during trawl selectivity experiments. The OS level in the fish was assessed by measuring lipid peroxidation (LPO), glutathione concentration (GSH), activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST), as well as acetylcholine esterase (AChE) in gills and liver. Round goby and red mullet caught in the Nessebar Bay showed clear signs of OS with the highest levels of LPO and GST activities, accompanied by the lowest AChE activities in both liver and gills. On the contrary, round goby caught near Maslen Nos (a region with good ecological conditions) were least affected by OS with low LPO and high GSH concentrations and SOD activity. There were no significant differences in the OS bioindicators of horse mackerel from the different localities. Sprat caught in Nessebar Bay, compared to those caught from the other localities, showed presence of OS indicated by lower GSH levels and relatively higher CAT, GPx and GST activities, accompanied by low AChE activity in gills. It can be concluded that round goby and red mullet were more vulnerable to OS induced by marine environmental factors than the horse mackerel and sprat. However, their antioxidant defense system allows them to tolerate and adapt to the environment of their habitats. Further studies are needed for the assessment of OS in important fish species in the Bulgarian part of the Black Sea.

Böbrek taşı hastalarda ESWL’ ye bağlı renal hasar üzerine nar suyunun önleyici etkisi

Objective: We aimed to show whether the antioxidant properties of pomegranate juice (PJ) show a protective effect against renal damage associated with oxidative stress caused by Extracorporeal Shock Wave Lithotripsy (ESWL) in patients who have undergone ESWL for kidney stones. Material and Methods: Ninety patients who were to undergo ESWL for kidney stones were included in the study and were divided into 3 groups with 30 patients each ESWL. Group 1 (control group) patients received only ESWL treatment. Group 2 (study group) patients were recommended to take 30 ml/kg/day pomegranate juice mixture orally for 2 days before ESWL. Group 3 (placebo group) patients were recommended to take 30 mg/kg/day water orally for 2 days before ESWL. All ESWL-treated patients received 2000 to 2500 shock waves at 18 to 24 in order to measure lipid peroxidation markers showing the DNA lesion associated with oxidative stress and to show tubular damage after ESWL, Results: There was a statistically significant mean increase of 52.39± 10.49 in 8-Hydroxy deoxyguanosine (8-OHdG) levels after treatment compared to pre-treatment levels in Group 1 (p&lt;0.01). There was a statistically significant mean increase of 13.16±7.71 and 33.24±12.82 in Groups 2 and 3, respectively (p&lt;0.01; p&lt;0.01, respectively) There was a statistically significant mean increase of 19.20±5.21 in N-acetyl-beta-D-glucosaminidase (NAG) levels after treatment compared to pre-treatment levels in Group 1 (p&lt;0.01). There was a statistically significant mean increase of 3.44±5.21 and 13.07±5.50 in Groups 2 and 3, respectively (p&lt;0.01; p&lt;0.01, respectively). Conclusion: Our study concluded that pomegranate juice (PJ) has protective effects against ESWL-related renal damage. Keywords: Antioxidant, kidney stones, lithotripsy, pomegranate juice.

Oxidative stress and its impact on skin, scalp and hair.

Oxidative stress is an unbalanced condition in which the tissues of the body are not sufficiently able to counteract either exogenous or endogenous sources of reactive oxygen species. Oxidative stress is strongly associated with ageing, both local and systemic, as well as a wide range of local health conditions. This review focuses on the oxidative stress data known for skin, scalp and hair. This oxidative stress may be the 'currency' by which an unhealthy scalp leads to deleterious consequences to the hair. The ramifications of this scalp oxidative stress to normal hair elongation, retention and replacement are discussed.

Antiseizure effects of Anacyclus pyrethrum in socially isolated rats with and without a positive handling strategy.

Aqueous extract of Anacyclus pyrethrum (AEAPR) is used in traditional medicine to treat epilepsy, but whether it has antiseizure properties has not been established. Because extracts of the plant have antioxidant properties, we hypothesized that it may be particularly potent in conditions associated with oxidative stress, in particular social isolation. We addressed these objectives in the pilocarpine experimental model of epilepsy using socially isolated rats maintaining contacts with (handled) and without (unhandled) positive handling strategy. Both groups were further divided into treated (AEAPR was added to the drinking water) and untreated groups. Continuous (24/7) electroencephalography (EEG) recordings started in the sixth week after status epilepticus (SE) with a predrug control period of 3weeks, followed by 3weeks of daily treatment with AEAPR or water, and finally a postdrug control period of 3weeks. At the end of the experimental procedure, we measured lipid peroxidation, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase activities in the hippocampus to assess oxidative stress. A. pyrethrum treatment significantly reduced seizure frequency by 51% and 57%, duration by 30% and 33%, and severity by 31% and 26% in isolated handled and unhandled rats, respectively. The beneficial effects on seizures were still present 3weeks after the end of the treatment. The treatment reduced lipid peroxidation as well as SOD, GPx, and catalase activities. We conclude that A. pyrethrum has antiseizure and antioxidant properties, even in social isolation conditions.

Lycopene minimizes skin toxicity and oxidative stress in patients treated with panitumumab-containing therapy for metastatic colorectal cancer

• Lycopene reduces ≥ G2 skin toxicity frequency in course of panitumumab therapy. • Lycopene prolongs time to appearance of ≥ G2 skin toxicity ( p = 0.0007 logrank test) • Lycopene protects tissues from oxidative stress due to panitumumab therapy. • Lycopene administration saves antioxidants consumption due to panitumumab therapy. Epidermal Growth Factor Receptor (EGFR) inhibition leads to the production of reactive oxygen metabolites causing skin inflammatory reactions. Anti-EGFR therapies are frequently associated with skin toxicities which often cause treatment delay and impairment to patient quality of life. Lycopene is a compound in the carotenoid group with an extreme antioxidant action which accumulates in the skin due to its hydrophobic structure. In a pilot study, we describe lactolycopene effectiveness in reducing skin toxicity and protecting tissues from oxidative stress in patients treated with panitumumab. Despite the limited number of patients, we show an absolute reduction of skin grade 2–3 toxicity in 41% of patients and 46% of panitumumab cumulative cycles in the experimental group versus placebo; lactolycopene administration was able to abolish malondialdehyde (MDA) production, a biomarker used to measure lipid peroxidation in the organism, and replenish antioxidant consumption in the course of anti-EGFR therapy. Trial registration: Clinicaltrials.gov NCT 03,167,268 (Pasto trial).