Levels Of Lipid Peroxidation Markers Research Articles

Protective Effect of Prunetin on Isoproterenol-Induced Myocardial Infarction in Wistar Rats via Biochemical Characterization.

The development of MI following ischemia damage is influenced by oxidative stress. Myocardial Infarction (MI) generates myocardial ischemia injury, which damages the cardiomyocytes. Ischemia builds up to a critical level over time in MI, causing permanent myocardial cell damage or death. The current study sought to determine whether Prunetin (PRU) could protect against Isoproterenol (ISO)-induced cardiac heart failure in rats by examining cardiac diagnostic markers, lipid peroxidation products, enzymatic and non-enzymatic antioxidant levels, and histological changes. PRU (20 mg/kg bwt) was orally administered for 19 days to rats, and after the treatment, ISO (85 mg/kg bwt) was subcutaneously administered with an intermission of 24 h for a couple of days to induce myocardial infarction on 20th and 21st days. ISO-treated rats exhibited considerable alterations in cardiac-sensitive markers in the serum. The levels of lipid peroxidation markers augmented drastically in the plasma and myocardium. Enzymatic antioxidant levels in erythrocytes and myocardium and the states of non-enzymatic antioxidants were diminished in the plasma and heart tissue of ISO-treated rats. The histopathological examination of heart tissue exhibited cardiac damage in ISO-induced rats. The oral administration of PRU significantly lowered the levels of lipid peroxidation and biochemical indicators, while significantly improving the antioxidant system function of ISO-interposed rats. In PRU-treated ISO-injected rats, histological examinations revealed suppressed myocardial destruction. Our research shows that oral pretreatment of PRU prevented ISO-induced oxidative stress in MI.

The Role of Oxidative Stress in Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Preclinical Studies.

Alcoholic Fatty Liver Disease (AFLD) is characterized by the accumulation of lipids in liver cells owing to the metabolism of ethanol. This process leads to a decrease in the NAD+/NADH ratio and the generation of reactive oxygen species. A systematic review and meta-analysis were conducted to investigate the role of oxidative stress in AFLD. A total of 201 eligible manuscripts were included, which revealed that animals with AFLD exhibited elevated expression of CYP2E1, decreased enzymatic activity of antioxidant enzymes, and reduced levels of the transcription factor Nrf2, which plays a pivotal role in the synthesis of antioxidant enzymes. Furthermore, animals with AFLD exhibited increased levels of lipid peroxidation markers and carbonylated proteins, collectively contributing to a weakened antioxidant defense and increased oxidative damage. The liver damage in AFLD was supported by significantly higher activity of alanine and aspartate aminotransferase enzymes. Moreover, animals with AFLD had increased levels of triacylglycerol in the serum and liver, likely due to reduced fatty acid metabolism caused by decreased PPAR-α expression, which is responsible for fatty acid oxidation, and increased expression of SREBP-1c, which is involved in fatty acid synthesis. With regard to inflammation, animals with AFLD exhibited elevated levels of pro-inflammatory cytokines, including TNF-a, IL-1β, and IL-6. The heightened oxidative stress, along with inflammation, led to an upregulation of cell death markers, such as caspase-3, and an increased Bax/Bcl-2 ratio. Overall, the findings of the review and meta-analysis indicate that ethanol metabolism reduces important markers of antioxidant defense while increasing inflammatory and apoptotic markers, thereby contributing to the development of AFLD.

Pharmacotherapeutic potential of ginkgetin against polystyrene microplastics-instigated testicular toxicity in rats: A biochemical, spermatological, and histopathological assessment.

Polystyrene microplastics (PSMPs) have emerged as a ubiquitous environmental toxicant that affects different organs including testes. Ginkgetin (GNG)is a biflavonoid that shows antioxidant properties. The current research was undertaken to evaluate the ameliorative potential of GNG against PSMPs-instigated testicular damages. Forty-eight albino rats (male) were randomly divided into 4 equal groups: control, PSMPs-treated group (0.01 mgkg-1), GNG + PSMPs-exposed group (25 mgkg-1 + 0.01 mgkg-1), and only GNG-supplemented group (25 mgkg-1). After 56days of treatment, it was revealed that PSMPs significantly reduced the activity of glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GSR), while concurrently augmented the levels of lipid peroxidation marker, i.e., malondialdehyde (MDA) along with reactive oxygen species (ROS). Rats administered with PSMPs showed a significant reduction in the spermatogenic indices (sperm count, viability, and motility), HOS coiled tail sperm along with increased sperm structural deformities, i.e., tail, head, and mid-piece. Additionally, PSMPs exposure decreased the levels of testosterone, luteinizing (LH), and follicle-stimulating hormones (FSH). Besides, administration of PSMPs reduced the steroidogenic enzymes (13β-HSD, StAR, and 17β-HSD) and Bcl-2 expression, while augmented the caspase-3 and Bax expression. PSMPs also elevated thelevels of inflammatory markers (IL-6, IL-1β, TNF-α, and NF-κB) and activity of COX-2 in the testes. Furthermore, PSMPs treatment induced various histopathological damages inthe testes of rats. Therefore, findings of the current study suggested that GNG effectively mitigated the PSMPs-induced testicular toxicity owing to its chemoprotective potential possibly through its anti-inflammatory, antioxidant, anti-apoptotic, and androgenic properties.

LIPID PEROXIDATION IN THE BLOOD OF MALES AND FEMALES WITH MYOCARDIAL INFARCTION AND DIABETES MELLITUS TYPE 2

Individuals with diabetes have a four-fold risk of developing coronary heart disease than those without diabetes. Dyslipidemia and hypertension associated with diabetes are additional risk factors for heart attack and myocardial infarctions. Oxidative stress induces many chronic diseases, especially diabetes and heart disease. Purpose: determination of lipid peroxidation markers in males and females with type 2 diabetes, individuals who have had myocardial infarctions, and individuals with type 2 diabetes and myocardial infarctions compared with healthy individuals. Methodology. The criteria for inclusion in the study were individuals with type 2 diabetes with a duration of at least 10 years, individuals with type 2 diabetes who had at least two myocardial infarcts, and healthy individuals (the control group of different genders), aged 35-71. In the obtained plasma, the level of lipid peroxidation (concentration of 2-thiobarbituric acid reacting substances) was assessed. Scientific novelty. Our study showed a significant increase in lipid peroxidation biomarker levels in all subjects compared to the control group. Males had a higher level of lipid peroxidation compared to females, indicating that men with type 2 diabetes and/or myocardial infarctions were more exposed to the harmful effects of oxidative stress. An increase in lipid peroxidation markers in the plasma of individuals with myocardial infarctions and diabetes compared to healthy individuals was observed. This may indicate the key importance of oxidative stress in the pathology of diabetes and myocardial infarctions. Analysis of multifactorial variance among a group with type 2 diabetes and myocardial infarction has shown the increase in the level of lipid peroxidation markers is influenced by the male gender. Conclusions. Increased plasma level of oxidative stress biomarkers was observed in both groups with myocardial infarctions and type 2 diabetes, as well as with diabetes and myocardial infarctions compared to the control group. In addition, a greater increase in lipid peroxidation in males compared to the female group was observed. The results obtained are another step in understanding the metabolic alterations in diabetes and myocardial infarction.

Comparison of the level of lipid peroxidative marker and antioxidants between preeclamptic and normotensive pregnant women

Preeclampsia is a complex multisystem disorder that is characterized by hypertension and proteinuria which is exclusively seen in human species. This disorder is a leading cause of maternal and fetal morbidity and mortality. It is seen that placental oxidative stress is involved in the etiopathogenesis of preeclampsia. This oxidative stress induces endothelial cell injury which in turn causes lipid peroxidation. Although the lipid peroxidation is counteracted by the action of several antioxidants.The aim of this study was to elucidate the changes in the level of lipid peroxidation markers and antioxidants in preeclamptic pregnant women that may contribute to the pathogenesis in preeclampsia. Fifty (50) pregnant women clinically diagnosed as preeclampsia were taken as subjects and an equal number of age matched, parity matched and gestation age matched healthy normotensive pregnant women were taken as controls for the study. This is the case-control hospital based study carried in the Department of Biochemistry, Pacific Institute of Medical Sciences (PIMS), Umarda, Udaipur (Raj.).Blood samples collected were estimated for Malondialdehyde (MDA) and Superoxide dismutase (SOD) using standard spectrophotometric method and Vitamin C and Uric acid using standard colorimetric method. Comparison between both the groups was done by Student’s t-test.The levels of MDA and uric acid were significantly elevated (p<0.001), and the levels of Vitamin C and SOD were significantly decreased (p<0.001) in preeclamptic pregnant women as compared to the normotensive pregnant women.The results of our study concluded that the increased levels of lipid peroxidation product (MDA) and depletion of antioxidant such as Vitamin C and SOD except uric acid in preeclamptic women may suggest that oxidative stress plays a key role in inducing oxidative stress and expression of preeclampsia.

Retraction Note to: Silibinin ameliorates arsenic induced nephrotoxicity by abrogation of oxidative stress, inflammation and apoptosis in rats

Arsenic (As) is an environmental and industrial pollutant that affects various organs in human and experimental animals. Silibinin is a naturally occurring plant bioflavonoid found in the milk thistle of Silybum marianum, which has been reported to have a wide range of pharmacological properties. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of As toxicity. Since kidney is the critical target organ of chronic As toxicity, we carried out this study to investigate the effects of silibinin on As-induced toxicity in the kidney of rats. In experimental rats, oral administration of sodium arsenite [NaAsO2, 5 mg/(kg day)] for 4 weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid, creatinine with a significant (p < 0.05) decrease in creatinine clearance. As also significantly decreased the levels of urea, uric acid and creatinine in urine. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant (p < 0.05) decrease in non-enzymatic antioxidants (total sulfhydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase), Glutathione metabolizing enzymes (glutathione reductase and glutathione-6-phosphate dehydrogenase) and membrane bound ATPases were also observed in As treated rats. Co-administration of silibinin (75 mg/kg day) along with As resulted in a reversal of As-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. The histopathological and immunohistochemical studies in the kidney of rats also shows that silibinin (75 mg/kg day) markedly reduced the toxicity of As and preserved the normal histological architecture of the renal tissue, inhibited the caspase-3 mediated tubular cell apoptosis and decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue. The present study suggests that the nephroprotective potential of silibinin in As toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in As-induced renal damage.

Biochemical markers of depression - an up-to-date review

IntroductionDepression or Major Depressive Disorder (MDD) is the most prevalent psychiatric disorder and a leading cause of disability worldwide. Currently affecting around 300 million people worldwide, depression is a major clinical, emotional, and socioeconomic strain for society. There is a growing interest in the biological underpinnings of depression, which are reflected by altered levels of biomarkers.ObjectivesThe aim of the study was to present an up-to-date review of potential MDD biomarkers.MethodsPubMed, Scopus, and Web of Science databases were searched.ResultsEnhanced inflammation has been reported in MDD, as reflected by increased concentrations of inflammatory markers – interleukin-6, C-reactive protein, tumor necrosis factor-α, and soluble interleukin-2 receptor. Dysregulation of the hypothalamus-pituitary-adrenals axis, along with increased cortisol levels, have also been reported in MDD. Oxidative and nitrosative stress also plays an important role in the pathophysiology of MDD. Notably, increased levels of lipid peroxidation markers are characteristic of MDD. Kynurenine metabolites, increased glutamate and decreased total cholesterol are also features of MDD. Finally, alterations in growth factors, with a significant decrease in brain-derived neurotrophic factor and an increase in fibroblast growth factor-2 and insulin-like growth factor-1 concentrations have also been found in MDD.ConclusionsA group of substances holds promise as reliable biomarkers for MDD. However, biomarker research in depression faces many difficulties, such as insufficient understanding of MDD etiopathogenesis, substantial heterogeneity of the disorder and low specificity of biomarkers. The construction of biomarker panels and their evaluation with use of new technologies may have the potential to overcome the above mentioned obstacles.DisclosureNo significant relationships.

Peripheral Markers of Depression.

Major Depressive Disorder (MDD) is a leading cause of disability worldwide, creating a high medical and socioeconomic burden. There is a growing interest in the biological underpinnings of depression, which are reflected by altered levels of biological markers. Among others, enhanced inflammation has been reported in MDD, as reflected by increased concentrations of inflammatory markers—C-reactive protein, interleukin-6, tumor necrosis factor-α and soluble interleukin-2 receptor. Oxidative and nitrosative stress also plays a role in the pathophysiology of MDD. Notably, increased levels of lipid peroxidation markers are characteristic of MDD. Dysregulation of the stress axis, along with increased cortisol levels, have also been reported in MDD. Alterations in growth factors, with a significant decrease in brain-derived neurotrophic factor and an increase in fibroblast growth factor-2 and insulin-like growth factor-1 concentrations have also been found in MDD. Finally, kynurenine metabolites, increased glutamate and decreased total cholesterol also hold promise as reliable biomarkers for MDD. Research in the field of MDD biomarkers is hindered by insufficient understanding of MDD etiopathogenesis, substantial heterogeneity of the disorder, common co-morbidities and low specificity of biomarkers. The construction of biomarker panels and their evaluation with use of new technologies may have the potential to overcome the above mentioned obstacles.

Toxicity of mercury on the brain: ability of extract of Pistacia atlantica regulated effect

Objective: The purpose of this study was to evaluate the neuroprotective effect of 150 mg / kg extract of the plant Pistacia atlantica against mercury-induced oxidative stress&#x0D; Methods: Hg was administered intraperitoneally (2,5 mg/kg body weight, one time a week), and P. atlantica and were given orally by gavage at a daily dose (150 mg/kg body weight) to rats for 32 days. 24 male adult Albinos Wistar rats were divided into four groups: group 1 Control, group 2 (HgCl2) group 3 (Hg + P. atlantica) and group 4 (P. atlantica). Paramatrical tests of oxidative stress and histological sections of the cerebral parenchyma. Results: Our results showed that the intraperitoneal injection of mercury chloride HgCl2 causes deleterious effects in the brain resulting in: a failure of redox status by disrupting the antioxidant defense system by a significant decrease in the activity of catalase glutathione peroxidase, glutathione-s-transferase and superoxide dismutase acetylcholinesterase and increase of the activity of the enzyme lactate dehydrogenase. The levels of lipid peroxidation markers were high in TBARS intoxicated rats with protein oxidation increased in the brain intoxicated by. The continuous use of mercury is also at the origin, in brain tissue However, supplementation of P. atlantica extract with mercury-treated rats attenuated some of the harmful and toxic effects of this metal. This clearly demonstrates the protective roles of this plant&#x0D; Keywords: mercury, Pistacia atlantica, Wistar rat, brain, antioxidant, neurotoxicity.

Protective Effect of Diosgenin on Streptozotocin Induced Diabetic Nephropathy in Experimental Rats

Diabetes mellitus is a multifactorial metabolic disorder associated with the diabetes related vascular diseases. Oxidative stress along with inflammation is the Key factor leading to diabetic complications. Present study was designed to investigate the protective role of diosgenin, a steroidal saponin, in diabetes induced early kidney injury and oxidative stress markers and histopathological changes in kidney of diabetic rats, induced by single intra-peritoneal injection of streptozotocin (55 mg/kg weight (b.w.). After 72 hrs, experimental rats received diosgenin at different doses (10, 20 and 40 mg/kg b.w.) once daily for four weeks. At the end of the experiment, diabetic rats showed a significant increase in the levels of plasma glucose, glycosylated hemoglobin with a significant decrease in insulin and total hemoglobin. The activities of antioxidant enzymes such as superoxide dismutase, catalase, reduced glutathione, and the levels of reduced glutathione were decreased while increases in the levels of lipid peroxidation markers were observed in kidney tissues of diabetic rats. Oral administration of diosgenin to diabetic rats considerably shrivelled the plasma glucose and exaggerated the endocrine level supported a dose dependent manner. Diosgenin at a dose of 40 mg/kg b.w. was more pronounced effect than the other two doses and used for further studies. All the manifestations observed in diabetic rats were significantly reversed to near normal at a dose of 40 mg/kg b.w. of diosgenin. These findings recommend that diosgenin may have a helpful role against excretory organ harm evoked by aerobic stress within the diabetic state.

Hepatoprotective and antioxidant activities of Dicranopteris linearis leaf extract against paracetamol-induced liver intoxication in rats

Context Dicranopteris linearis L. (Gleicheniaceae) leaves have been reported to exert hepatoprotective activity. Objective The hepatoprotective and antioxidant effects of ethyl acetate partition of D. linearis (EADL) are investigated. Materials and methods EADL was subjected to antioxidant and anti-inflammatory studies, and phytochemical analyses. In vivo study involved six groups (n = 6) of overnight fasted Sprague Dawley rats. The test solutions [10% DMSO (normal), 10% DMSO (negative), 200 mg/kg silymarin (positive) or EADL (50, 250 or 500 mg/kg)] were administered orally once daily for 7 consecutive days followed by oral vehicle (only for normal) or hepatotoxic induction using 3 g/kg paracetamol (PCM). Results EADL exerted ≈ 90% radical scavenging effects based on the DPPH and superoxide anion radical scavenging assays, high antioxidant capacity in the oxygen radical absorbance capacity assay (≈ 555,000 units), high total phenolic content (≈ 350 mg GAE/100 g extract) (p < 0.05), but low anti-inflammatory effect. EADL also attenuated PCM-induced liver intoxication as indicated by reduced level of serum liver enzymes; increased activity of endogenous enzymatic antioxidant (superoxide dismutase – 8.3 vs. 4.0 U/g tissue; catalase – 119 vs. 52 U/g tissue) and; reduced level of lipid peroxidation marker (2.7 vs. 5.0 µM). Preliminary screening of EADL revealed the presence of saponins, tannins and flavonoids with further HPLC analysis demonstrating the presence of rutin and quercetin. Discussion and conclusion EADL exerted hepatoprotective and antioxidant activities; thus, these data support the potential use of D. linearis as a new source for future hepatoprotective drug development.

Dysfunction of inflammatory pathways in adolescent female patients with anorexia nervosa

BackgroundThe pathogenesis of Eating Disorders is still unknown. However, a growing body of evidence shows that there are changes in cytokine levels and an alteration in the stress response in patients with anorexia nervosa (AN). For this reason, we decided to test whether there are differences in immune parameters involved in the regulation of the inflammatory response between female adolescents with AN and healthy adolescents. MethodsThe sample 27 drug-naïve AN patients the study sample included 27 AN patients at a very early stage of the disease and 23 healthy controls. Plasma and peripheral blood mononuclear cells (PBMCs) were obtained for biochemical study. ResultsPlasma levels of the pro-inflammatory cytokines TNF-α and IL-1β were significantly increased in patients with AN, while the levels of prostaglandins PGE2 (proinflammatory) and 15d-PGJ2, (anti-inflammatory) were lower compared with controls. Protein expression in PBMCs of cyclooxygenase-2 (COX-2) and the activated forms of the mitogen-activated protein kinases p38 and ERK were also increased in the AN group. Expression levels of the anti-inflammatory factor peroxisome proliferator-activated receptor gamma (PPARγ) were significantly decreased in patients. Plasma levels of lipid peroxidation markers –TBARS- were not increased in patients with AN.Components of the biochemical inflammatory response (COX-2, PGE2, TBARS, 15d-PGJ2, ERK, p65 NFκB) and glucocorticoid receptor –GR- expression and the scores on the impulsivity measures in the BARRATT, EDI and BITE questionnaires showed a significant correlation within the AN patients group. ConclusionsThe results for female adolescent patients with AN indicate that there is a dysfunction of intra- and intercellular inflammatory pathways characterized by higher levels of pro-inflammatory parameters in plasma and a decrease in one of the controlling cytoplasmic-nuclear pathways implicated in their modulation (i.e. PPARγ) with, at this very early stage of the disease, no effect on oxidative stress markers plasma levels. Most notably, higher severity of illness (restrictive and purging behaviour) correlated with higher levels of inflammatory markers.

Radioprotective efficacy of dieckol against gamma radiation-induced cellular damage in hepatocyte cells.

Naturally occurring antioxidants prevent or delay the harmful effect of free radical formation and radioprotection. The present study aimed to investigate the radioprotective effect of dieckol, a naturally occurring marine bioactive phenolic compound on lipid peroxidation and antioxidant status, DNA damage, and inflammation in gamma-radiation-induced rat primary hepatocytes. Isolated hepatocyte cells exposed to gamma-radiation showed an increased level of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) accompanied with the decrease in the activities of enzymatic (SOD, CAT, and GPx) and non-enzymatic (vitamin C, vitamin E, and GSH) antioxidants associated with increased DNA damage coupled with upregulation of inflammatory proteins (NF-κB and COX-2) compared to control. Treatment of dieckol (5, 10, 20μM) reduces the γ-radiation-induced toxicity and the associated pro-oxidant and antioxidant imbalance as well as decreasing the DNA damage (tail length, tail moment, %DNA in a tail and olive tail moment) and inflammation in hepatocyte cells. These findings indicate that treatment of dieckol offers protection against γ-radiation-induced cellular damage in the liver cells.

Baseline levels of antioxidant activities in Mytilus galloprovincialis along the coast of Cape Town, South Africa

Antioxidant activities in Mytilus galloprovincialis were determined from samples collected at Scarborough, Hout Bay, Green Point, Milnerton and Bloubergstrand in Cape Town, South Africa. Antioxidant enzyme activity was determined by measuring CAT, SOD and GSH. The total antioxidant capacity was measured using FRAP and ORAC, while the content and lipid peroxidation marker levels of CDs and TBARS. Antioxidant activities and responses in mussels varied between sites with significant correlations for 85% and 71% of all antioxidant measurements made for Fe and Zn, respectively. The oxidative stress results reported here are novel for the region and indicated that mussels in Cape Town do not have (relatively) high levels of antioxidant activities as a result of exposure to metals. The research undertaken suggests that antioxidant responses was an appropriate biomarker of exposure to metals but more environmental parameters should be considered when interpreting antioxidant responses in the natural environment.

Oxidative stress in epilepsy

This article contains an analysis of clinical and experimental studies in which oxidative stress is considered as a possible mechanism in the pathogenesis of epilepsy. Oxidative stress occurs as a result of brain damage after epileptic seizures and may later cause epileptogenesis. Patients with epilepsy showed a high level of lipid peroxidation markers, while the activity of antioxidant defense system was low. The level of oxidative stress was shown to be significantly higher in epileptics with associated mental disorders and in patients with refractory epilepsy. Further study of oxidative stress in epilepsy may play the key role in the treatment of this disease.

The Electrical Stimulation of the Bed Nucleus of the Stria Terminalis Causes Oxidative Stress in Skeletal Muscle of Rats.

Recent studies indicate that activation of hypothalamus-pituitary-adrenocortical axis (HPA) plays the crucial role in stress response, while several lines of evidence mark the bed nucleus of the stria terminalis (BST) as a major mediator of the HPA axis responses to stress. The purpose of this study was to investigate the influence of the corticosterone flux induced by the electrical stimulation of BST on markers of free radical damage of lipids and proteins and antioxidant enzyme activity in skeletal muscle of rats. The male Wistar rats were used and assigned to one of three groups: sham-operated (SHM; n = 6), two-week (ST2; n = 6), and four-week stimulated (ST4; n = 5) groups. Blood, soleus, and extensor digitorum longus muscles were collected. The chronic, 4-week electrical stimulation of the BST evokes increased plasma corticosterone concentration, which resulted in oxidative stress in skeletal muscles. We found higher level of lipid peroxidation markers, lower level of protein oxidation marker, and elevated antioxidant enzyme activity in both muscles. Our findings have also potential implication showing that reaction to the long-term “psychological stress” may lead to free radical damage of muscle.

Hens ranked as highly feed efficient have an improved albumen quality profile and increased polyunsaturated fatty acids in the yolk1

The shelf life of eggs that contain elevated levels of polyunsaturated fatty acids (PUFA) is compromised due to the relative instability and therefore greater potential for lipid peroxidation of unsaturated fatty acids (FA). Poultry that is highly feed efficiency (HFE) exhibits higher systemic levels of antioxidant enzymes and therefore may produce eggs with improved albumen quality and favorable FA profiles that are stable over time. We tested the hypothesis that HFE-laying hens produce eggs with improved internal egg quality and a favorable yolk FA profile prior to and following storage. Following an initial screening phase (7 wk) using 140 Isa Brown layers (28 wk old), the 10 most efficient (FCR < 1.99 ± 0.05) and the 10 least efficient (FCR > 2.30 ± 0.05) hens were identified and designated as HFE and low feed efficiency (LFE) groups, respectively. Internal quality and composition were determined on eggs (n = 10 per group) stored at 15 °C for 0, 14, and 28 d. At 0, 14, and 28 d, the albumen weight, albumen height, Haugh unit (HU), and albumen:yolk ratio of eggs from the HFE group were significantly higher (P < 0.01), whereas the eggs from the LFE group had heavier (P < 0.01) yolk than the HFE group. After 28-d storage, the yolk color score of the LFE group was lower (paler; P < 0.05) compared with that of the HFE group. The relative proportions of total PUFA and the ratio of total PUFA and total saturated fatty acids (SFA) were higher (P < 0.05) in HFE group of eggs. The LFE group of eggs contained higher (P < 0.05) levels of lipid peroxidation marker (thiobarbituric acid reactive substances; TBARS) values both in fresh and in stored eggs. The results suggest that HFE hens produce eggs with greater albumen quality and higher levels of yolk PUFA both at lay and after storage.

L-carnitine mitigates UVA-induced skin tissue injury in rats through downregulation of oxidative stress, p38/c-Fos signaling, and the proinflammatory cytokines

UVA comprises more than 90% of the solar UV radiation reaching the Earth. Artificial lightening lamps have also been reported to emit significant amounts of UVA. Exposure to UVA has been associated with dermatological disorders including skin cancer. At the molecular level, UVA damages different cellular biomolecules and triggers inflammatory responses. The current study was devoted to investigate the potential protective effect of L-carnitine against UVA-induced skin tissue injury using rats as a mammalian model. Rats were distributed into normal control group (NC), L-carnitine control group (LC), UVA-Exposed group (UVA), and UVA-Exposed and L-carnitine-treated group (UVA-LC). L-carnitine significantly attenuated UVA-induced elevation of the DNA damage markers 8-oxo-2′-deoxyguanosine (8-oxo-dG) and cyclobutane pyrimidine dimers (CPDs) as well as decreased DNA fragmentation and the activity of the apoptotic marker caspase-3. In addition, L-carnitine substantially reduced the levels of lipid peroxidation marker (TBARS) and protein oxidation marker (PCC) and significantly elevated the levels of the total antioxidant capacity (TAC) and the antioxidant reduced glutathione (GSH) in the skin tissues. Interestingly, L-carnitine upregulated the level of the DNA repair protein proliferating cell nuclear antigen (PCNA). Besides it mitigated the UVA-induced activation of the oxidative stress-sensitive signaling protein p38 and its downstream target c-Fos. Moreover, L-carnitine significantly downregulated the levels of the early response proinflammatory cytokines TNF-α, IL-6, and IL-1β. Collectively, our results highlight, for the first time, the potential attenuating effects of L-carnitine on UVA-induced skin tissue injury in rats that is potentially mediated through suppression of UVA-induced oxidative stress and inflammatory responses.

Strain- and sex-dependent pulmonary toxicity of waterpipe smoke in mouse.

Waterpipe smoking is emerging as a form of tobacco smoking, but its lung health/risks is not known. It has been shown that different mouse strains show differences in susceptibility to tobacco smoke. However, the effect of waterpipe smoke (WPS) exposure and strain differences in susceptibility to oxidative and inflammatory responses is not known. Here, we showed acute WPS exposure induced oxidative stress and inflammatory response in C57BL/6J and BALB/cJ mouse strains. WPS exposure induced inflammatory cell influx (neutrophils and T‐lymphocytes) in bronchoalveolar lavage fluid (BAL fluid), which varied among mouse strains. Proinflammatory cytokines release differed among both the strains, but was significantly increased in C57BL/6J mice. Myeloperoxidase levels in BAL fluid were increased significantly in both the strains. Total reduced glutathione (GSH) level was decreased, whereas the level of oxidized or glutathione disulfide (GSSG) increased in lungs of both the strains. Similarly, the level of lipid peroxidation markers, 15‐isoprostane (plasma), malondialdehyde and 4‐hydroxy‐2‐nonenal (lung homogenates) were increased by WPS. Our data suggest that, oxidative stress and inflammatory responses are influenced by strain characteristics during acute WPS exposure. Overall, C57BL/6J mice showed more susceptibility to oxidative stress and inflammatory responses compared to BALB/cJ mice. Acute WPS mediated pulmonary toxicity is differentially regulated in different mouse strains.

Beneficial Protective Effect of Troxerutin on Nickel-Induced Renal Dysfunction in Wistar Rats.

Nickel (Ni) is an important environmental toxicant that can cause cancer and cardiovascular disease. The aim of this study was to examine the protective effects of troxerutin (Txn) Ni-induced renal dysfunction in rats using biochemical and histopathological approaches. Nickel (20 mg/kg body weight [b.w.]/day) was administered intraperitoneally (i.p.) for 20 days. Renal damage from Ni toxicity was evident from the changed levels of serum and urinary markers in Ni-treated rats. The levels of lipid peroxidation markers also significantly increased, while the levels of nonenzymatic and enzymatic antioxidants significantly decreased in the kidney of Ni-intoxicated rats. Troxerutin was administered orally (100 mg/kg b.w.) for 20 days along with Ni, resulting in a reversal of Ni-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. Histopathological studies in the kidneys of rats also showed that troxerutin (100 mg/ kg b.w.) markedly reduced the toxicity of Ni and preserved the normal histological architecture of the renal tissue. The present study results suggest the nephroprotective potential of Txn in Ni toxicity, which might be due to its antioxidant and metal-chelating properties.