End Product Of Lipid Peroxidation Research Articles

α-Tocopherol inhibits atherogenesis and improves cardiac function in mice independently of its antioxidant properties.

The impact of α-tocopherol on atherosclerosis is unclear and controversial. While some studies suggest potential benefits, such as antioxidant properties that may reduce oxidative stress, other studies indicate no significant preventive effects. The intricate interplay of various factors, including dosage, individual differences, and study methodologies, contributes to the ongoing uncertainty surrounding α-tocopherol's role in atherosclerosis. Further research is needed to clarify its impact and establish clearer guidelines. Therefore, we aimed to evaluate the impact of α-tocopherol on atherogenesis in ApoE-/- fibrillin (Fbn)1C1039G/+ mice, which is a unique mouse model of advanced atherosclerosis with typical features, such as large necrotic cores, high levels of inflammation, and intraplaque neovascularization, that resemble the unstable phenotype of human plaques. ApoE-/- Fbn1C1039G+/- mice were fed a western-type diet (WD) supplemented with a high dose of α-tocopherol (500 mg/kg diet), while control mice were fed a WD containing a low dose of α-tocopherol (50 mg/kg diet). The high dose of α-tocopherol reduced plaque thickness and necrotic core area in the right common carotid artery (RCCA) after 24 weeks WD. Moreover, α-tocopherol decreased plaque formation and intraplaque neovascularization in the RCCA. In addition to its antiatherogenic effect, chronic supplementation of α-tocopherol improved cardiac function in ApoE-/- Fbn1C1039G/+ mice. However, chronic supplementation of α-tocopherol did not decrease lipid peroxidation. On the contrary, α-tocopherol acted as a prooxidant by increasing plasma levels of oxidized LDL and plaque malondialdehyde, an end product of lipid peroxidation. Our data indicate that α-tocopherol inhibits atherogenesis and improves cardiac function independent of its antioxidant properties.

Pseudocannabinoid H4CBD Reduces Cardiac Damage Indicator 4HNE in OLETF (Otsuka Long Evans Tokushima Fatty) Rats

Cardiovascular disease (CVD) is a leading cause of death globally and MetS is an associated precursor of CVD. Of the 6 known cluster factor conditions of MetS, obesity, and poor glucose tolerance are known to contribute to high lipid peroxidation, which can contribute to the generation of damaging free radical species and a pro-oxidant system. Cannabidiol (CBD) is a known antioxidant and a growing understanding of CBD analogs and pseudocannabinoids, like H4CBD, implicate similar antioxidant effects. However, little is known about the effects of CBD analogs on MetS-associated cardiac tissue damage. To better understand these effects during extreme metabolic dysfunction, 41-weeks-old animals were assigned into three groups, (n=8/group): (1) one-lean-strain control, Long Evans Tokushima Otsuka (LETO), (2) untreated OLETF, and (3) OLETF + H4CBD (200 mg/kg/day x 4 weeks). Our hypothesis focuses on the prospect that ongoing treatment with H4CBD in a MetS model using Otsuka Long-Evans Tokushima Fatty (OLETF) rats will reduce indicators of lipid peroxidation including 4-hydroxynonenal (4HNE), a toxic end product of lipid peroxidation. After the 4-week treatment, cardiac tissue was analyzed for 4-hydroxynonenal (4HNE) protein expression. We found that H4CBD decreased cardiac 4HNE protein expression in treated OLETF rats by 68% (p<0.05) compared to OLETF control, which indicates H4CBD attenuated cardiac lipid peroxidation overall. Although the 4-week treatment of H4CBD was not suffcient to ameliorate MetS-associated hypertension, the reduction of 4HNE suggests that the attenuation of cardiac damage is independent of arterial pressure. These data indicate that H4CBD and its derivatives hold promise for therapeutic use in managing CVD and related metabolic syndrome-associated pathologies. Undergraduate Research Training Initiative for Student Enhancement (U-RISE), Center for Medical Cannabis Research. 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.

Improvement of Antioxidative Activity of Broiler Muscles after Dietary Modulation with Selenium and Methionine

Abstract The objective of the study was to compare the antioxidative capacity of broiler chicken breast and leg muscles after dietary modulation with selenium (Se) and methionine (Met). Free radical scavenging (ABTS, DPPH) and iron reduction (FRAP) activities were determined as the total antioxidative potential (TEAC), as well the enzyme activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), in relation to concentrations of lipid peroxidation end products (TBARS). Analyses were performed on breast m. pectoralis superficialis and profundus individually and together. The studied leg muscles included biceps femoris, gastrocnemicus, iliotiobialis, peroneus longus, sartorius, semimembranosus, semitendinosus and all leg muscles together. Flex broiler chickens were fed diets supplemented with 6.7, 8.2, 9.7 and 11.2 g DL-methionine/kg feed and Se as sodium selenite and selenized yeast at 0.26, 0.38 and 0.50 mg Se/kg. Greater TEAC and enzyme activities were observed in leg than in breast muscles. Selenium did not change TEAC in muscles sets, but improved antiradical capacity in the pectoralis major and minor, sartorius and biceps femoris. The highest level of methionine increased TEAC in individual leg muscles. Selenium and methionine at the highest concentrations increased SOD activity in the entire group and individual muscles, while Se raised GPx activity. In conclusion, the diet supplementation with selenium and high concentrations of methionine had a greater impact on the antioxidative potential of individual than the whole set of chicken breast and leg muscles. The positive effect of the studied diet modulation could raise the quality and extend the shelf-life of fresh chicken meat.

Hepatoprotective effect of methanol fruit extract of Punica granatum L in highly active antiretroviral therapy-induced toxicity in Wistar rats

Prolonged use of Highly Active Antiretroviral Therapy (HAART) has been linked to toxicity, particularly hepatotoxicity. There are few effective drugs for HAART patients that promote hepatic cell regeneration and prevent liver injury. Therefore, the purpose of this study was to investigate the hepato-protective activity of Methanol fruit extract of Punica granatum (MFEPG) in HAART-administered rats. Thirty rats weighing between 150–200 g were randomly divided into six groups and each group comprised of five rats. Distilled water was given to the rats in group one. Only HAART was given to the rats in group two. MFEPG at doses of 100 and 400 mg/kg was given to the rats in groups three and four. MFEPG dosages of 100 and 400 mg/kg along with HAART were given to the rats in groups five and six, respectively. All treatments were via oral gavage daily for 40 days. Under halothane anesthesia, all rats were sacrificed on day 41. Liver tissues were utilized for lipid peroxidation marker; Malondialdehyde (MDA), antioxidant enzymes; Superoxide dismutase (SOD) and Catalase (CAT) and histological evaluation, while blood samples were examined for biochemical parameters (AST, ALT, ALP, Total cholesterol, Total protein, and Albumin). The HAART-treated group exhibited a significantly higher amount of the lipid peroxidation end product; MDA, and significantly lower levels of antioxidant enzymes; SOD, and CAT. Liver enzymes and total cholesterol were significantly increased with a significant reduction in Total protein and Albumin levels in the HAART-treated group. Conversely, the liver function biomarkers were returned to normal levels in the HAART and MFEPG-treated groups. Histopathological studies revealed that when HAART-exposed rats were treated with MFEPG, both the biochemical and histological results significantly improved. Thus, the antioxidant activity of MFEPG provides protection against HAART-induced liver oxidative damage. More research is needed to determine the safety of using MFEPG in humans.

The protective effect of PL 1-3 on D-galactose-induced aging mice.

The aging population has become an issue that cannot be ignored, and research on aging is receiving increasing attention. PL 1-3 possesses diverse pharmacological properties including anti-oxidative stress, inhibits inflammatory responses and anti-apoptosis. This study showed that PL 1-3 could protect mice, especially the brain, against the aging caused by D-galactose (D-gal). D-gal could cause oxidative stress, inflammation, apoptosis and tissue pathological injury and so on in aging mice. The treatment of PL 1-3 could increase the anti-oxidative stress ability in the serum, liver, kidney and brain of aging mice, via increasing the total antioxidant capacity and the levels of anti-oxidative defense enzymes (superoxide dismutase, glutathione peroxidase, and catalase), and reducing the end product of lipid peroxidation (malondialdehyde). In the brain, in addition to the enhanced anti-oxidative stress via upregulating the level of the nuclear factor erythroid 2-related factor 2 and heme oxygenase 1, PL 1-3 could improve the dysfunction of the cholinergic system via reducing the active of acetylcholinesterase so as to increase the level of acetylcholine, increase the anti-inflammatory and anti-apoptosis activities via downregulating the expressions of pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and pro-apoptosis proteins (Bcl-2 associated X protein and Caspase-3) in the D-gal-induced aging mice, to enhance the anti-aging ability via upregulating the expression of sirtuin 1 and downregulating the expressions of p53, p21, and p16. Besides, PL 1-3 could reverse the liver, kidney and spleen damages induced by D-gal in aging mice. These results suggested that PL 1-3 may be developed as an anti-aging drug for the prevention and intervention of age-related diseases.

Effect of Flaxseed Supplementation in the Maternal Diet During Early Lactation on the Oxidative Status of Sows and Growth of Piglets

The present study was conducted on 21 crossbred Large White Yorkshire sows to assess the effect of flaxseed supple mentation on oxidative stress in sows and growth of piglets. All sows were equally allocated into three groups. Group 1 served as the control and followed their normal feeding schedule. Group 2 and group 3, in addition to their normal feed ing schedule, were supplemented with flaxseed at a rate of 0.5% and 1.0% of the dry matter, respectively. Blood samples were collected 15 days prior to farrowing, on the day of farrowing (day 0), at weekly intervals until day 28 of lactation and at monthly intervals during gestation to assess the oxidative status in each sow. Body weight and weight gain in each piglet was measured during lactation period. The assessment of oxidative stress in blood was done through estimations of malondialdehyde (MDA), end product of lipid peroxidation. No changes (P>0.05) in MDA concentrations were mani fested at any of the days measured during lactation and gestation in sows of all the groups. Similarly, there was no effect of flaxseed treatment on superoxide dismutase (SOD) levels in all sows at any of the days measured during lactation period (P>0.05) as well as during gestation period (days 30-90). In the current farrowing, the piglets exhibited a steady increase (P<0.05) in bodyweight as well as weight gain in all groups from day 0 until day 28 of lactation. No effect (P>0.05) of flax seed fed to sows on litter weight and weight gain was noticed until day 21 of lactation, However, the effect of treatment was evinced on day 28 of lactation compared to control group. In conclusion, flaxseed supplementation had no impact on MDA and SOD concentrations in sows; nevertheless a treatment effect was noticed on body weight and weight gain in piglets.

Biological Activity of Novel Pyrrole Derivatives as Antioxidant Agents Against 6-OHDA Induced Neurotoxicity in PC12 Cells.

Neuroinflammation and oxidative stress are critical factors involved in the pathogenesis of Parkinson's disease (PD), the second most common progressive neurodegenerative disease. Additionally, lipid peroxidation end products contribute to inflammatory responses by activating pro-inflammatory genes. Lipid peroxidation occurs as a result of either the overproduction of intracellular reactive oxygen species (ROS) or the reaction of cyclooxygenases (COXs). In this study, we examined the role of 1,5-diaryl pyrrole derivatives against the neurotoxic effects of 6-hydroxydopamine (6-OHDA) in a cellular model of PD. PC12 cells were pre-treated with compounds 2-(4-chlorophenyl)-5-methyl-1-(4-(trifluoromethoxy)phenyl)-1H-pyrrole (A), 2-(4-chlorophenyl)-1-(4-methoxyphenyl)-5-methyl-1H-pyrrole (B), and 1-(2-chlorophenyl)-2-(4-chlorophenyl)-5-methyl-1H-pyrrole (C), respectively, 24 h before exposure to 6-OHDA. We conducted various assays, including 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT), ROS, and lipid peroxidation assays, Hoechst staining, Annexin V/PI, Western blotting analysis and ELISA method, to assess the neuroprotective effects of pyrrole derivatives on 6-OHDA-induced neurotoxicity. Our results demonstrated that apoptosis induction was inhibited by controlling the lipid peroxidation process in the in vitro model following pre-treatment with compounds A, B, and, somehow, C. Furthermore, compounds A and C likely act by suppressing the COX-2/PGE2 pathway, a mechanism not attributed to compound B. These findings suggest that the novel synthetic pyrrolic derivatives may be considered promising neuroprotective agents that can potentially prevent the progression of PD.

Green Preparation, Characterization, Wound Healing Assessment, and Histopathological Evaluation of Vitamin A Encapsulated in Niosome and Solid Lipid Nanoparticle

Background: The purpose of the current work was to manufacture vitamin A (Vit A) niosome and solid lipid nanoparticle (SLN) using an ultrasonic approach and to evaluate its effect on wound healing. Methods: The nanoparticles were prepared through an ultrasonication technique and characterized by dynamic light scattering (DLS), and transmission electron microscopy (TEM). Further, the nanoparticles were evaluated for their various parameters such as pH, viscosity, spreadability, stability, in-vitro drug release study, in-vitro cytotoxicity, and in-vivo wound healing. Results: TEM confirmed the spherical nature of the Vit A-niosome and SLN. The Vit A formulations (niosome and SLN) were stable in the accelerated stability test (freeze-thaw cycle). Vit A release from the SLN gel and niosome gel was significantly higher (almost 70 and 80%, respectively) than simple Vit A gel. According to the animal study, the wound healing closure in the Vit A niosomal gel and Vit A SLN gel was greater than the other groups during the 21 days after surgery (P < 0.05) and was close to each other over time and on day 21. Based on histological data, wounds treated with Vit A niosome gel and Vit A-SLN gel had more collagen than the other groups. MDA malondialdehyde (MDA, an end-product of lipid peroxidation) significantly decreased in the Vit A-niosome and Vit A-SLN gel group after 21 days, while glutathione peroxidase (GPx), superoxide dismutase (SOD, an endogenous antioxidant), and hydroxyproline levels demonstrated an increase. Conclusion: The findings of this study revealed that the prepared Vit A nano-formulations could be used as a possible and safe nano-vesicle for Vit A cutaneous delivery thus potentially opening up new prospects for the treatment of wound disorders.

Thiobarbituric Acid Reactive Substances (TBARS) in Dog’s Hair as a Sign of Oxidative Stress – Preliminary Study

Abstract Various endogenous and exogenous factors influence the occurrence of oxidative stress in all organisms, as well as in dogs. An increase in reactive oxygen species (ROS) concentration and the occurrence of oxidative stress can lead to changes in the structure of proteins, lipids, and DNA. The level of oxidative stress can be determined by measuring the end products of lipid peroxidation known as reactive substances of thiobarbituric acid (TBARS) of which malondialdehyde (MDA) is the most important. The concentration of MDA can be easily measured in various tissues and body excretions, but also by a non-invasive method of hair sampling. In this research, we have collected dog hair in grooming saloons, fluorometrically measured TBARS levels and compared the obtained values with factors such as breed, sex, age, passive smoking, sterilization, and season. No significant difference between sterilized and non-sterilized dogs was observed. The intensity of lipid peroxidation differed between the sexes, dog breeds, status of smoking by owner and exposure to UV radiation.

Effects of caseous lymphadenitis agent (corynebacterium pseudotuberculosis) isolated from superficial abscesses of sheep on oxidative stress factors

In this study, it was aimed to determine the incidence of Corynebacterium pseudotuberculosis (C. pseudotuberculosis) in caseous lymphadenitis cases in superficial lymph nodes of sheep and to evaluate its effect on oxidative stress factors. Thus, it was aimed to determine the early diagnosability of superficial and visceral caseous lymphadenitis cases and to prevent the spread of diseases and related economic losses. A total of 103 sheep, 50 of which were healthy and 53 of which had caseous lymphadenitis, were evaluated in the study. Microbiological examinations were performed by taking 3-5 ml of pyogenic aspirate from the superficial lymph nodes of sheep with caseous lymphadenitis. Blood samples were taken from sheep with C. pseudotuberculosis isolated in microbiological examinations and the levels of oxidative stress factors were determined. C. pseudotuberculosis was isolated in 23 of the pyogenic aspirates of 53 sheep with caseous lymphadenitis. When sheep isolated from C. pseudotuberculosis were compared with healthy sheep, it was determined that there was a statistically significant decrease in the levels of antioxidant molecules such as GSH-pX (14.62%), GSH (23.81%), SOD (4.70%), CAT (22.23%) (p˂0.001). The level of toxic malondialdehyde (MDA) (18.62%), the end product of lipid peroxidation, was found to be statistically significantly increased in sheep isolated from C. pseudotuberculosis (p˂0.001). As a result, it was determined that oxidative stress factors showed statistically significant variability in cases of superficial caseous lymphadenitis (caused by C.pseudotuberculosis). For this reason, by determining the levels of oxidative stress factors in suspected herds, it was possible to make early diagnosis of the superficial and visceral forms of caseous lymphadenitis, and a basis was established for future studies.

Lipid peroxidation-derived modification and its effect on the activity of glutathione peroxidase 1

Oxidative stress and the resulting lipid peroxidation are associated with various pathological states, including neurodegenerative diseases and cancer. The end products of lipid peroxidation, such as 4-oxo-2(E)-nonenal (ONE), 4-hydroxy-2(E)-nonenal (HNE), and methylglyoxal (MG), exert several biological effects through modification of various cellular components, including DNA and proteins. Glutathione peroxidase 1 (GPx1) is an intracellular antioxidant enzyme that uses glutathione (GSH) to reduce a variety of peroxides, thereby modulating cellular oxidative stress and redox-mediated responses. GPx1 contains nucleophilic amino acids at its active (one Sec) and GSH-binding (four Arg and one Lys) sites. We found that lipid peroxidation-derived reactive aldehydes (ONE, HNE, and MG) modified the GSH-binding site, resulting in the inhibition of GPx1 activity. Mass spectrometry-based proteomic analysis identified the sites modified by each aldehyde (ONE, 14 sites; HNE, 7 sites; MG, 9 sites). The GSH-binding sites modified were as follows: ONE, Arg57, 103, 184, and 185; HNE, Lys91; MG, Arg103. Upon incubation of GPx1 with each aldehyde, ONE reduced GPx1 activity more significantly than did HNE or MG in a dose- and time-dependent manner. The addition of GSH to GPx1 3 h after incubation with ONE prevented further inhibition by trapping ONE as a ONE-GSH adduct. However, the activity of GPx1 was not restored to the initial level, indicating that ONE modified GPx1 irreversibly. This study suggests that oxidative damage to lipids, resulting in the formation of reactive aldehydes, can amplify cellular oxidative stress via direct inactivation of GPx1, which increases the production of intracellular peroxides.

Preclinical evaluation of a gel composition based on a flavonoid complex for the treatment of periodontal diseases in orthodontic patients

The aim of the work was a preclinical assessment of acute toxicity, skin resorptive, irritant effects, cumulative and catalase activity, as well as sensitizing properties of the local gel composition “Benzidaflaziverdine” (GCB) used for the treatment of periodontal diseases in orthodontic patients. Materials and methods. 119 animals were involved in the experiment, assigned to seven main and two control groups. GCB was administered intragastrically in doses of 300–600 mg/kg and intradermally of 200 μg into the outer surface of the ear. The native solution of GCB was applied to the skin and mucous membranes, administered orally by the method of “subchronic toxicity” and to the surface of the chorioallantoic membrane (CAM) of chicken embryos. The intensity of lipid peroxidation (LPO) was assessed by the level of diene conjugates (DCs) and malondialdehyde (MDA), and the antioxidant system by catalase activity. The specific leukocyte agglomeration reaction (SLAR), the specific leukocyte lysis reaction, and neutrophil damage indicators were used. Results. The median lethal dose LD50 for rats and mice of both sexes exceeded 5000 mg/kg. The irritant effect of GCB on the mucous membranes was manifested by hyperemia on the second day. Symptoms of irritation disappeared after 3–4 days without medical intervention. An analysis of the CAM blood vessels after exposure to GCB in two observations at the 120th second showed the beginning of hemorrhages. In one observation, GCB caused minor hemorrhages at the 300th second of the experiment. It was found that the coefficient of GCB irritant action was 5 (the mean score of Me (Q1; Q3) was 5 (4; 5)). The coefficient of cumulation (Kcum) exceeded 8.2. An insignificant increase in the median or mean values of catalase enzyme activity, DCs, and the amount of LPO end product such as MDA was observed compared to the control group animals. The SLAR test indicated the development of a delayed-type allergic reaction under the influence of GCB in a 1:10 dilution. One-hundred-fold dilution did not cause significant changes in the indicator in the main group compared to the control one. Conclusions. GCB belongs to the 4th class of toxicity – practically non-toxic substances, does not have sex- and species sensitivity, has weak cumulative activity, minimal effect on the system of LPO. GCB can be recommended for the use in clinical periodontology for medical support of orthodontic patients.

Dietary Olive Leaf Extract Differentially Modulates Antioxidant Defense of Normal and Aeromonas hydrophila-Infected Common Carp (Cyprinus carpio) via Keap1/Nrf2 Pathway Signaling: A Phytochemical and Biological Link.

Olive leaves are an immense source of antioxidant and antimicrobial bioactive constituents. This study investigated the effects of dietary incorporation of olive leaf extract (OLE) on the growth performance, hematobiochemical parameters, immune response, antioxidant defense, histopathological changes, and some growth- and immune-related genes in the common carp (Cyprinus carpio). A total of 180 fish were allocated into four groups with triplicate each. The control group received the basal diet without OLE, while the other three groups were fed a basal diet with the OLE at 0.1, 0.2, and 0.3%, respectively. The feeding study lasted for 8 weeks, then fish were challenged with Aeromonas hydrophila. The results revealed that the group supplied with the 0.1% OLE significantly exhibited a higher final body weight (FBW), weight gain (WG%), and specific growth rate (SGR) with a decreased feed conversion ratio (FCR) compared to the other groups (p < 0.05). An increase in immune response was also observed in the fish from this group, with higher lysosome activity, immunoglobulin (IgM), and respiratory burst than nonsupplemented fish, both before and after the A. hydrophila challenge (p < 0.05). Similarly, the supplementation of the 0.1% OLE also promoted the C. carpio's digestive capacity pre- and post-challenge, presenting the highest activity of protease and alkaline phosphatase (p < 0.05). In addition, this dose of the OLE enhanced fish antioxidant capacity through an increase in the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and decreased hepatic lipid peroxidation end products (malondialdehyde-MDA), when compared to the control group, both pre- and post-infection (p < 0.05). Concomitantly with the superior immune response and antioxidant capacity, the fish fed the 0.1% OLE revealed the highest survival rate after the challenge with A. hydrophila (p < 0.05). A significant remarkable upregulation of the hepatic sod, nrf2, and protein kinase C transcription levels was detected as a vital approach for the prevention of both oxidative stress and inflammation compared to the infected unsupplied control group (p < 0.05). Interestingly, HPLC and UPLC-ESI-MS/MS analyses recognized that oleuropein is the main constituent (20.4%) with other 45 compounds in addition to tentative identification of two new compounds, namely oleuroside-10-carboxylic acid (I) and demethyl oleuroside-10-carboxylic acid (II). These constituents may be responsible for the OLE exerted potential effects. To conclude, the OLE at a dose range of 0.66-0.83 g/kg w/w can be included in the C. carpio diet to improve the growth, antioxidant capacity, and immune response under normal health conditions along with regulating the infection-associated pro-inflammatory gene expressions, thus enhancing resistance against A. hydrophila.

Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation

The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction and/or exposure to IR resulted in a significant decrease in the serum levels of T3 and T4 associated with increased levels of lipid peroxidation end product, malondialdehyde (MDA), and nitrites (NO) in the brain tissue homogenate. Also, hypothyroidism and /or exposure to IR markedly enhance the endoplasmic reticulum stress by upregulating the gene expressions of the protein kinase RNA-like endoplasmic reticulum kinase (PERK), activated transcription factor 6 (ATF6), endoplasmic reticulum-associated degradation (ERAD), and CCAAT/enhancer-binding protein homologous protein (CHOP) in the brain tissue homogenate associated with a proapoptotic state which indicated by the overexpression of Bax, BCl2, and caspase-12 that culminates in brain damage. Meanwhile, the PTU and /or IR-exposed rats treated with MEE reduced oxidative stress and ERAD through ATF6. Also, the MEE treatment prevented the Bax and caspase-12 gene expression from increasing. This treatment in hypothyroid animals was associated with neuronal protection as indicated by the downregulation in the gene expressions of the microtubule-associated protein tau (MAPT) and amyloid precursor protein (APP) in the brain tissue. Furthermore, the administration of MEE ameliorates the histological structure of brain tissue. In conclusion, MEE might prevent hypothyroidism-induced brain damage associated with oxidative stress and endoplasmic reticulum stress.

Assessment of Oxidative Stress by the Estimation of Lipid Peroxidation Marker Malondialdehyde (MDA) in Patients with Chronic Periodontitis: A Systematic Review and Meta-Analysis.

The present systematic review and meta-analysis aimed to assess the oxidative stress-mediated lipid peroxidation end product malondialdehyde (MDA) in periodontitis using the available literature. An electronic literature search was performed for the published articles from 2000 to 2022 in PubMed (MeSH), Science Direct, Wiley Online library, and cross-reference using specific keywords. The literature search identified 1,166 articles. After analyzing the abstracts of the obtained articles, the articles were excluded for the following reasons: duplicate studies (n = 395) and not relevant to the research question (n = 726). The remaining 45 articles were chosen for full-text evaluation. Finally, the present qualitative synthesis selected 34 articles that met the inclusion criteria for evaluation and removed the articles which did not meet the required criteria (n = 11). Out of these, 16 articles had coherent data for quantitative synthesis. The meta-analysis used the standardized mean differences method at a 95% confidence interval by random-effects model. The periodontitis group displayed significantly higher MDA levels (P < 0.001) in gingival crevicular fluid, saliva, and serum samples of the studies analyzed than the healthy control. The analyzed studies showed significantly higher MDA levels in various biological samples of patients with periodontitis, supporting the role of elevated oxidative stress and consequent lipid peroxidation in periodontitis.

Influence of liposomal thiosulfonate drug on the blood parameters of cows suffering catarrhal mastitis

Diseases of the mammary gland in cows are of multi-factor nature, which significantly complicates their control and treatment. One of the factors influencing development of mastitis is bacterial microflora. Because of limited use of antibiotics, development of novel alternative antmicrobial drugs is of great relevance. Therefore, the objective of the study was identifying the effect of an ethyl-thiosulfanilate-based liposomal drug on the hematological and biochemical parameters of blood of the cows suffering catarrhal mastitis. The animals were three times intramuscularly injected with the liposomal drug in the dose of 0.04 mL/kg of body weight. Blood from the cows was taken from the jugular vein on the day prior to administration of the drug, and also on the 3rd and 7th days after its application. During the bacterial study of the secretion of udder of sick cows, we collected 51 bacterial isolates, in which dominated Staphylococcus aureus (27.5%) and Streptococcus spp. (21.6%). In blood of the sick cows, we found higher number of leukocytes, increases in the concentrations of circulating immune complexes, lipid hydroperoxides, and ketone derivatives of oxidative modification of proteins. At the same time, we observed decreases in the number of lymphocytes and concentration of protein and the bactericidal activity of blood serum. Administration of the complex liposomal drug had a normalizing effect on the analyzed parameters of the cows. This was evidenced by 9.4% decrease in the total number of leukocytes, 18.5% decrease in the content of circulating immune complexes, 9.3% increase in lymphocytes, and 13.6% increase in the level of total protein. In the sick cows, the drug enhanced the bactericidal (by 35.4%) and lysozymic (by 36.3%) activities of blood serum, glutathione peroxidase activity, and increased the content of reduced glutathione. On the seventh day after injecting the drug into blood of the cows, we saw decrease in the level of intermediate and end products of lipid peroxidation and derivatives of oxidative modification of proteins. Therefore, the complex ethyl-thiosulfanilate-based liposomal drug promoted reduction of metabolic homeostasis of the organism, had positive effect on the activity of natural defense mechanisms in the organism and can be recommended for the treatment of cows with catarrhal mastitis.

Dragon Fruit Peel Waste (Hylocereus undatus) as a Potential Ingredient for Reducing Lipid Peroxidation, Dietary Advanced Glycation End Products, and Starch Digestibility in Cookies.

Excessive consumption of cookies has been linked to harmful health outcomes owing to the presence of refined carbohydrates and heat-induced toxicants including end products of lipid peroxidation and dietary advanced glycation end products (dAGEs). To address this issue, this study explores the addition of dragon fruit peel powder (DFP), which is rich in phytochemicals and dietary fibers, to cookies as a potential solution to mitigate their adverse effects. The results indicate that adding DFP at 1%, 2%, and 5% w/w of raw cookie dough significantly improves the total phenolic and betacyanin contents and antioxidant activity, as evidenced by increased ferric-reducing antioxidant power. DFP incorporation also led to reductions in malondialdehyde and dAGEs (p < 0.05). Furthermore, the starch digestibility, hydrolysis index, and predicted glycemic index were all reduced in the presence of DFP, with the latter estimate being due to the higher content of undigested starch. Incorporating DFP in cookies resulted in significant changes in their physical properties, including texture and color. However, sensory evaluation indicates that the overall acceptability of the cookies was not negatively impacted by the addition of up to 2% DFP, suggesting that it is a viable option for enhancing the nutritional value of cookies without compromising their palatability. These findings suggest that DFP is a sustainable and healthier ingredient that can improve the antioxidant capacity of cookies while also mitigating the harmful effects of heat-induced toxins.

Correlation between Superoxide Dismutase (SOD) with Malondialdehyde (MDA) level in blood plasma of seborrheic keratosis

Introduction: Seborrheic keratosis (SK) is a benign tumor of the epidermis, its development is associated with various hypotheses, but none came out as the main culprit. A few study results regarding the oxidative stress strongly associated with skin tumors have been reported. Superoxide dismutase (SOD) is a potent protective enzymatic antioxidant. Malondialdehyde (MDA) is the end product of lipid peroxidation produced by free radicals in the body. Increased levels of MDA usually accompany low levels of antioxidants. Methods: This study was an observational analytic study with a cross-sectional method involving 42 seborrheic keratosis subjects based on inclusion and exclusion criteria. We recorded the gender, age, family history, and occupation of the subjects. Diagnosis of seborrheic keratosis was made based on history taking and clinical examination—measurement of SOD level by ELISA method and MDA levels by TBARS method. The Spearman correlation test was measured and was considered significant if the p-value was &lt;0.05. Results: Seborrheic keratosis was more common in females (92.9%), with the most common age group being 40 ̶ 50 years old (57.1%), had a family history of SK (26.2%), and worked in agriculture, forestry, and fisheries (26.2%). The average blood plasma SOD level was 1.68 mmol/L, and the blood plasma MDA level was 181.19 U/L. The correlation coefficient between blood plasma SOD levels and blood plasma MDA levels was -0.393, with a significant value of p=0.01. This study showed that the lower the SOD level, the higher the MDA level in the blood plasma of seborrheic keratosis. Conclusion: There is a significant correlation between SOD and MDA levels in the blood plasma of seborrheic keratosis subjects.

Urinary 15-F2t-Isoprostane Concentrations in Dogs with Liver Disease.

Isoprostanes are stable end products of lipid peroxidation that can be used as markers of oxidative stress. It was previously reported that a cohort of dogs with various liver diseases had increased urinary isoprostane concentrations compared to healthy control (HC) dogs. The aim of this study was to measure and report urinary isoprostane concentrations in dogs with different types of liver diseases. Urine was collected from 21 HC dogs and from 40 dogs with liver disease, including 25 with chronic hepatitis (CH), 7 with steroid hepatopathy (SH), and 8 with a congenital portosystemic shunt (CPSS). In this prospective, observational study, urinary 15-F2t-isoprostane (F2-IsoP) concentrations were measured by liquid chromatography/mass spectrometry and normalized to urinary creatinine concentrations. Concentrations were compared between groups using a Kruskal-Wallis test followed by Dunn's multiple comparisons tests. Significance was set at p < 0.05. The median (range) urinary F2-IsoP to creatinine ratios (ng/mg UCr) were 3.6 (2.2-12.4) for HC dogs, 5.7 (2.4-11.3) for dogs with CH, 4.8 (2.4-8.6) for dogs with SH, and 12.5 (2.9-22.9) for dogs with CPSS. CPSS dogs had significantly higher urinary F2-IsoP concentrations than HC dogs (p = 0.004), suggesting increased oxidative stress among this cohort.

Effect of Pravastatin on Levels of Malondealdehyde (MDA) And Endothelin-1 (ET-1) Preeclampsia Model Rats

Introduction: Pravastatin is known to have a number of pleiotropic effects including reducing endothelial dysfunction, anti-inflammatory, antioxidants, conangiogenic, and antitrombotic. Pravastatin through the pleitropic effect is expected to be one of the alternative therapies to prevent preeclampsia. The limited strategy for prevention and treatment of preeclampsia is due to the unknown etiology and pathogenesis. These two markers are thought to contribute to the occurrence of preeclampsia although they cause it in two different pathways. MDA is a marker of oxidative stress as an end product of lipid peroxidation. ET-1 is a vasoconstrictor that plays a role in the pathogenesis of preeclampsia through increasing anti-angiogenic properties. Aim: to determine the effect of pravastatin on serum levels of MDA and ET-1 in preeclampsia rat models. Methods: This study consisted of 5 groups; negative control/ K(-) consisted of normal pregnant rats, positive control/ K(+) consisted of rat model of preeclampsia (rat model of preeclampsia induced by administration of L-NAME at a dose of 125 mg/kg BW/day since gestational age 13-19 days), treatment groups 1, 2, and 3 (rat model of preeclampsia given pravastatin with 3 different doses; 2 mg/day (P1), 4 mg/day (P2) and 8 mg/day(P3)) at 13-19 days of gestation. The rat model of preeclampsia was determined based on blood pressure &gt; 140/90 with urine protein &gt; +1. After termination, blood was drawn to measure serum MDA and ET-1 levels. Results: Serum levels of MDA and ET-1 were decreased in groups P2 and P3 compared to groups K(+). Statistically, there was a significant difference in the mean levels of MDA (p=0.001) and ET-1 (p=0.000) between each group. Conclusion: Pravastatin can prevent preeclampsia by decreasing MDA and ET-1.