Effect of dietary supplementation of organic and inorganic Se on performance and antioxidant response in commercial broiler chickens.

1. The study was carried out to determine the effects of supplementing organic (OG) or inorganic (IOG) Se to record the performance, immune and anti-oxidant response in broiler chickens.2. One-day-old Vencobb-400 (50.1 ± 0.84 g; n = 280) male broiler chicks were allocated randomly into seven treatments to give eight replicates containing five chicks each and housed in deep littered floor pens (76 cm × 91 cm) for a period of 42 d.3. The control diet (CD) was formulated without any Se supplementation (diet I), CD plus 0.15, 0.30 or 0.45 mg/kg OG Se (diets II, III and IV, respectively) and CD plus 0.15, 0.30 or 0.45 mg/kg IOG Se (diets V, VI and VII, respectively).4. Feed intake (FI), body weight gain (BWG), immune variables and mRNA expression profile of hepatic selenoproteins (SepW, GSHPx1, TrxR and GSHPx3) genes were determined. The BWG, FI and feed conversion ratio did not differ among various dietary treatments.5. The lipid peroxidation and activity of RBC catalase were lower (P < 0.05) in groups fed diets supplemented OG Se compared to those fed IOG Se and CD. The activity of GSH Px was higher among the groups fed diet supplemented OG Se compared to those groups fed OG Se and CD. However, supplementing diets with OG or IOG Se did not affect humoral or cell mediated immune responses.6. The expression levels of SepW were higher (P < 0.01) among the groups supplemented with OG Se. Expression levels of GSH-Px1, TrxR and GSHPx3 were higher (P < 0.01) among the groups supplemented with OG Se compared to those groups fed IOG Se or CD.7. Supplementing OG Se improved the activities of anti-oxidant enzymes and hepatic expression of selenoproteins genes in the present study. However, supplementing OG or IOG Se did not affect growth performance and immune variables in broiler chickens.

Sustainable synthesis of microwave-assisted IONPs using Spinacia oleracea L. for control of fungal wilt by modulating the defense system in tomato plants.

BACKGROUND: Changing climate enhances the survival of pests and pathogens, which eventually affects crop yield and reduces its economic value. Novel approaches should be employed to ensure sustainable food security. Nano-based agri-chemicals provide a distinctive mechanism to increase productivity and manage phytopathogens, with minimal environmental distress. In vitro and in greenhouse studies were conducted to evaluate the potential of green-synthesized iron-oxide nanoparticles (IONPs) in suppressing wilt infection caused by Fusarium oxysporum f. sp. lycospersici, and improving tomato growth (Solanum lycopersicum) and fruit quality. RESULTS: Various microwave powers (100-1000 W) were used to modulate the properties of the green-synthesized IONPs, using spinach as a starting material. The IONPs stabilized with black coffee extract were substantively characterized using X-ray diffraction analysis (XRD), Fourier-transform infrared spectroscopy, dielectric and impedance spectroscopy, X-ray photoelectron spectroscopy (XPS), scanning and transmission electron microscopy (SEM and TEM, respectively), and magnetization analysis. XRD revealed a cubic magnetite (Fe3O4) phase with super-paramagnetic nature, detected at all microwave powers. The binding energies of Fe 2p3/2 (710.9 eV) and Fe 2p1/2 (724.5 eV) of Fe3O4 NPs were confirmed using XPS analysis at a microwave power of 1000 W. Uniform, spherical/cubical-shaped particles with an average diameter of 4 nm were confirmed using SEM and TEM analysis. A significant reduction in mycelial growth and spore germination was observed upon exposure to different IONP treatments. Malformed mycelium, DNA fragmentation, alternation in the cell membrane, and ROS production in F. oxysporum indicated the anti-microbial potential of the IONPs. The particles were applied both through the root (before transplantation) and by means of foliar application (after two weeks) to the infected seedlings. IONPs significantly reduced disease severity by an average of 47.8%, resulting in increased plant growth variables after exposure to 12.5 µg/mL of IONPs. Analysis of photosynthetic pigments, phenolic compounds, and anti-oxidant enzymes in the roots and shoots showed an increasing trend after exposure to various concentrations of IONPs. Correspondingly, lycopene, vitamin C, total flavonoids, and protein content were substantially improved in tomato fruits after treatment with IONPs. CONCLUSION: The findings of the current investigation suggested that the synthesized IONPs display anti-fungal and nutritional properties that can help to manage Fusarium wilt disease, resulting in enhanced plant growth and fruit quality.

Neutralization of IL-17 and treatment with IL-2 protects septic arthritis by regulating free radical production and antioxidant enzymes in Th17 and Tregs: An immunomodulatory TLR2 versus TNFR response.

Septic arthritis is a destructive joint disease caused by Staphylococcus aureus. Synovial inflammation involved Th17 proliferation and down regulation of Treg population, thus resolution of inflammation targeting IL-17 may be important to control arthritis. Endogenous inhibition of IL-17 to regulate arthritic inflammation correlating with Th17/Treg cells TLR2 and TNFRs are not done. The role of SOD, CAT and GRx in relation to ROS production during arthritis along with expression of TLR2, TNFR1/TNFR2 in Th17/Treg cells of mice treated with IL-17A Ab/ IL-2 were studied. Increased ROS, reduced antioxidant enzyme activity was found in Th17 cells of SA infected mice whereas Treg cells of IL-17A Ab/ IL-2 treated group showed opposite effects. Neutralization of IL-17 after arthritis cause decreased TNFR1 and increased TNFR2 expression in Treg cells. Thus, neutralization of IL-17 or IL-2 treatment regulates septic arthritis by enhancing anti-inflammatory properties of Treg via antioxidant balance and modulating TLR2/TNFR response.

Anti-inflammatory, anti-oxidant and hepatoprotective effects of lactoferrin in rats.

Carbon tetrachloride (CCl4) is a strong hepatotoxic agent. The ability of the anti-inflammatory agent, lactoferrin (LF), to alleviate hepatic inflammation in a Wistar rat model administered with carbon tetrachloride (CCl4) was examined. Thirty male Wistar rats were segregated into 5 groups (6 rats per group): Control group, LF group (300 mg LF/kg b. wt daily for three weeks), CCl4 group (1 ml CCl4/kg b. wt once orally), LF-protected group (300 mg LF/kg b. wt daily for 3 weeks followed by 1 mL CCl4/kg b. wt once orally), and LF-treated group (1 mL CCl4/kg b.wt once orally followed by 300 mg LF/kg b. wt orally every day for three weeks). Erythrogram, leukogram, activity of oxidative stress markers (Superoxide dismutase [SOD], Glutathione peroxidase [GPx], and Malondialdehyde [MDA]), and expression of hepatic paraoxonase-1 (PON1), interleukin (IL)-1ß, and IL-10 mRNA were determined. Histopathological examination of the hepatic tissue was carried out. CCl4 caused liver injury, loss of liver antioxidant activity of SOD and GPx, and a significant increase in the level of malondialdehyde in the serum. Moreover, CCl4 induced up-regulation of hepatic pro-inflammatory (IL-1ß) factors, and down-regulation of anti-inflammatory (IL-10 and PON1) factors. Based on histopathological examination, the hepatic tissues had severe inflammation and were damaged. However, LF mitigated the liver damage, oxidative stress, and hepatotoxicity caused by CCl4. Overall, these results suggest that LF-mediated immunological mechanisms alleviate CCl4-induced hepatic toxicity and provide a novel perspective on the potential use of LF for prophylactic and therapeutic applications in treating liver diseases.

Cannabidiol on 5-FU-induced oral mucositis in mice.

PURPOSE: The aim of this study was to evaluate the clinical, histological, hematological, and oxidative stress effects of cannabidiol (CBD) in mice with induced oral mucositis. METHODS: We used 90 mice of the CF-1 strain in which oral mucositis was induced using a protocol with 5-fluorouracil (5-FU) chemotherapy. The animals were divided randomly into 10 study groups. Three groups were treated with different doses of CBD (3, 10, and 30 mg/kg), while 2 were control groups (positive control: 5-FU + mechanical trauma + placebo; and negative control: mechanical trauma + placebo), and 2 experimental times were studied (4 and 7 days). All treatments were by intraperitoneal administration. RESULTS: In the clinical evaluation, the groups treated with CBD showed less severity of oral lesions compared with the positive control at both experimental times. The intensity of the inflammatory response was also lower in the groups treated with this drug, but there was no statistically significant difference when compared with the positive control. With regard to erythrocyte, leukocyte, and platelet counts and anti-oxidant enzyme activity, the groups treated with CBD showed better results, but only some of these variables showed statistically significant differences. CONCLUSIONS: CBD seems to exert an anti-inflammatory and anti-oxidant activity favoring a faster resolution of oral mucositis in this animal model.

Short-Term Neonatal Oral Administration of Oleanolic Acid Protects against Fructose-Induced Oxidative Stress in the Skeletal Muscles of Suckling Rats.

Nutritional manipulations in the neonatal period are associated with the development of negative or positive health outcomes later in life. Excessive fructose consumption has been attributed to the increase in the global prevalence of metabolic syndrome (MetS) and the development of oxidative stress. Oleanolic acid (OA) has anti-diabetic and anti-obesity effects. We investigated the protective potential of orally administering OA in the neonatal period, to prevent fructose-induced oxidative stress, adverse health outcomes and maturation of the gastrointestinal tract (GIT) in suckling rats. Seven-day old Sprague-Dawley rats (N = 30) were gavaged daily with 10 mL/kg of: distilled water (DW), oleanolic acid (OA; 60 mg/kg), high fructose solution (HF; 20% w/v), or OAHF for 7 days. On day 14, tissue samples were collected to determine clinical health profiles, hepatic lipid content, and activity of anti-oxidant enzymes. Furthermore, biomarkers of oxidative stress and anti-oxidant capacity in the skeletal muscles were assessed. The gastrointestinal tract (GIT) morphometry was measured. Rats in all groups grew over the 7-day treatment period. There were no significant differences in the terminal body masses, GIT morphometry, surrogate markers of general health, liver lipid content across all treatment groups (p < 0.05). Neonatal fructose administration decreased the activity of catalase, depleted GSH and increased lipid peroxidation. However, the level of GSH and catalase activity were improved by neonatal OA treatment. Short-term oral OA administration during the critical developmental period protects against fructose-induced oxidative stress without adverse effects on health outcomes associated with MetS or precocious development of the GIT in suckling male and female rats.

DNA methylation in the central and efferent limbs of the chemoreflex requires carotid body neural activity.

KEY POINTS: The mechanisms underlying long-term (30 days) intermittent hypoxia (LT-IH)-evoked DNA methylation of anti-oxidant enzyme (AOE) gene repression in the carotid body (CB) reflex pathway were examined. LT-IH-treated rats showed increased reactive oxygen species (ROS) levels in the CB reflex pathway. Administration of a ROS scavenger or CB ablation blocked LT-IH-evoked DNA methylation and AOE gene repression in the central and efferent limbs of the CB reflex. LT-IH increased DNA methyltransferase (Dnmt) activity through upregulation of Dnmt1 and 3b proteins by ROS-dependent inactivation of glycogen synthase kinase 3ß (GSK3ß) by Akt. A pan-Akt inhibitor prevented LT-IH-induced GSK3ß inactivation, elevated Dnmt protein expression and activity, AOE gene methylation, sympathetic activation and hypertension. ABSTRACT: Long-term exposure to intermittent hypoxia (LT-IH; 30 days), simulating blood O2 profiles during sleep apnoea, has been shown to repress anti-oxidant enzyme (AOE) gene expression by DNA methylation in the carotid body (CB) reflex pathway, resulting in persistent elevation of plasma catecholamine levels and blood pressure. The present study examined the mechanisms by which LT-IH induces DNA methylation. Adult rats exposed to LT-IH showed elevated reactive oxygen species (ROS) in the CB, nucleus tractus solitarius (nTS) and rostroventrolateral medulla (RVLM) and adrenal medulla (AM), which represent the central and efferent limbs of the CB reflex, respectively. ROS scavenger treatment during the first ten days of IH exposure prevented ROS accumulation, blocked DNA methylation, and normalized AOE gene expression, suggesting that ROS generated during the early stages of IH activate DNA methylation. CB ablation prevented the ROS accumulation, normalized AOE gene expression in the nTS, RVLM, and AM and blocked DNA methylation, suggesting that LT-IH-induced DNA methylation in the central and efferent limbs of the CB reflex is indirect and requires CB neural activity. LT-IH increased DNA methyl transferase (Dnmt) activity through upregulation of Dnmt1 and 3b protein expression due to ROS-dependent inactivation of glycogen synthase kinase 3ß (GSK3ß) by protein kinase B (Akt). Treating rats with the pan-Akt inhibitor GSK690693 blocked the induction of Dnmt activity, Dnmt protein expression, and DNA methylation, leading to normalization of AOE gene expression as well as plasma catecholamine levels and blood pressure.

Relationship between antioxidant defense in Acanthamoeba spp. infected lungs and host immunological status.

The role of oxidative stress in the pathogenicity of acanthamoebiasis is an important aspect of the intricate and complex host-parasite relationship. The aim of this experimental study was to determine oxidative stress through the assessment of lipid peroxidation product (LPO) levels and antioxidant defense mechanism in Acanthamoeba spp. lung infections in immunocompetent and immunosuppressed hosts. In Acanthamoeba spp. infected immunocompetent mice we noted a significant increase in lung lipid peroxidation products (LPO) at 8 days and 16 days post infection (dpi). There was a significant upregulation in lung LPO in immunocompetent and immunosuppressed mice infected by Acanthamoeba spp. at 16 dpi. The superoxide dismutase activity decreased significantly in lungs in immunosuppressed mice at 8 dpi. The catalase activity was significantly upregulated in lungs in immunocompetent vs. immunosuppressed group and in immunocompetent vs. control mice at 16 dpi. The glutathione reductase activity was significantly lower in immunosuppressed group vs. immunosuppressed control at 24 dpi. We found significant glutathione peroxidase downregulation in immunocompetent and immunosuppressed groups vs. controls at 8 dpi, and in immunosuppressed vs. immunosuppressed control at 16 dpi. The consequence of the inflammatory response in immunocompetent and immunosuppressed hosts in the course of experimental Acanthamoeba spp. infection was the reduction of the antioxidant capacity of the lungs resulting from changes in the activity of antioxidant enzymes. Therefore, the imbalance between oxidant and antioxidant processes may play a major role in pathology associated with Acanthamoeba pneumonia.

Nyctanthes arbor-tristis leaf extract ameliorates hyperlipidemia- and hyperglycemia-associated nephrotoxicity by improving anti-oxidant and anti-inflammatory status in high-fat diet-streptozotocin-induced diabetic rats.

Type 2 diabetes is a multifactorial disorder coupled with impaired glucose tolerance, diminished insulin sensitivity and hyperlipidemia. Incessant hyperglycemia and hyperlipidemia led a towering risk to develop cardiovascular hitches with end-stage renal failure. Leaves of Nyctanthes arbor-tristis L. (NAT) (family: Oleaceae) is traditionally used by tribes of Assam for various ailments without proper scientific validation and appropriate mechanism of action for its activity. Hence, we aimed to evaluate the mechanism involved in the hypoglycemic and hypolipidemic effects of NAT leaves in high-fat diet (HFD)-streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley rats were fed with in-house prepared high-fat diet (HFD) for a period of 4 weeks to create insulin resistance. Streptozotocin was injected intraperitoneally to these rats to cause ß-cell destructions to create a model of type 2 diabetes. Our results have shown that NAT extract has a dose-dependent hypoglycemic and hypolipidemic activity in controlling the early biochemical parameters of kidney and lipids. Moreover, the extract has anti-oxidant and anti-inflammatory activities which were more pronounced at a dose of 400 mg/kg body weight. NAT treatment group also restored the normal architecture of the kidney and aorta tissue. GC-MS data analysis revealed the presence of several active compounds which are directly or indirectly responsible for its anti-diabetic and anti-hyperlipidemic activity. The apparent mechanism of NAT for its nephroprotection may be due to the suppression of hyperglycemia-mediated oxidative stress and amelioration of inflammatory cascades allied with NF-kB activation.

Epigenetic regulation of redox state mediates persistent cardiorespiratory abnormalities after long-term intermittent hypoxia.

KEY POINTS: The effects of short-term (ST; 10 days) and long-term (LT; 30 days) intermittent hypoxia (IH) on blood pressure (BP), breathing and carotid body (CB) chemosensory reflex were examined in adult rats. ST- and LT-IH treated rats exhibited hypertension, irregular breathing with apnoea and augmented the CB chemosensory reflex, with all these responses becoming normalized during recovery from ST- but not from LT-IH. The persistent cardiorespiratory responses to LT-IH were associated with elevated reactive oxygen species (ROS) levels in the CB and adrenal medulla, which were a result of DNA methylation-dependent suppression of genes encoding anti-oxidant enzymes (AOEs). Treating rats with decitabine either during LT-IH or during recovery from LT-IH prevented DNA methylation of AOE genes, normalized the expression of AOE genes and ROS levels, reversed the heightened CB chemosensory reflex and hypertension, and also stabilized breathing. ABSTRACT: Rodents exposed to chronic intermittent hypoxia (IH), simulating blood O2 saturation profiles during obstructive sleep apnoea (OSA), have been shown to exhibit a heightened carotid body (CB) chemosensory reflex and hypertension. CB chemosensory reflex activation also results in unstable breathing with apnoeas. However, the effect of chronic IH on breathing is not known. In the present study, we examined the effects of chronic IH on breathing along with blood pressure (BP) and assessed whether the autonomic responses are normalized after recovery from chronic IH. Studies were performed on adult, male, Sprague-Dawley rats exposed to either short-term (ST; 10 days) or long-term (LT, 30 days) IH. Rats exposed to either ST- or LT-IH exhibited hypertension, irregular breathing with apnoeas, an augmented CB chemosensory reflex as indicated by elevated CB neural activity and plasma catecholamine levels, and elevated reactive oxygen species (ROS) levels in the CB and adrenal medulla (AM). All these effects were normalized after recovery from ST-IH but not from LT-IH. Analysis of the molecular mechanisms underlying the persistent effects of LT-IH revealed increased DNA methylation of genes encoding anti-oxidant enzymes (AOEs). Treatment with decitabine, a DNA methylation inhibitor, either during LT-IH or during recovery from LT-IH, prevented DNA methylation, normalized the expression of AOE genes, ROS levels, CB chemosensory reflex and BP, and also stabilized breathing. These results suggest that persistent cardiorespiratory abnormalities caused by LT-IH are mediated by epigenetic re-programming of the redox state in the CB chemosensory reflex pathway.

Dietary omega-3 but not omega-6 fatty acids down-regulate maternal dyslipidemia induced oxidative stress: A three generation study in rats.

BACKGROUND: Maternal nutrition modulates fetal metabolic programming and development later. Maternal dyslipidemia effects on oxidative stress (OS) in offsprings and its modulation by dietary fatty acids over generations remains to be elucidated. The objective of present study was to assess the long-term (three generations) effect of omega-3 fatty acids on OS under dyslipidemia. METHODS: Weanling female Wistar rats were fed with control diet (7% lard), high fat diet (35% lard, HFL), high fat with fish oil (21% fish oil + 14% lard, HFF), high fat with canola oil (21% canola oil + 14% lard, HFC) and high fat with sunflower oil (21% sunflower oil + 14% lard, HFS). Following 60 days feeding, the female rats were mated with sexually matured males (fed normal chow diet) and continued with the above diet regimen during pregnancy and lactation. The pups after lactation were continued with their maternal diet for 60 days and subjected to mating and feeding trial as above for two generations. Serum lipid profiles, OS markers (lipid peroxidation, nitric oxide release and protein carbonyl) and antioxidant defence enzymes (catalase, SOD, glutathione peroxidase and glutathione transferase) were assessed in serum, liver and uterus of rats fed on experimental and control diets for three generations. RESULTS: Feeding HFL diet increased blood lipids, OS and lowered the antioxidant enzymes activity in serum, liver and uterus (p < 0.05). The reduction in the antioxidant enzymes in HFL group were higher in third followed by second generation compared to first generation (p < 0.05). Omega-3 fatty acids prevented the dyslipidemia induced loss of antioxidant enzyme activities in serum, liver and uterus. CONCLUSIONS: Our data show for the first time that offsprings born to dyslipidemic mothers' exhibit diminished enzymatic antioxidant defence and its progressive reduction in future generation, and dietary omega-3 fatty acids restore the enzymatic antioxidant defence in offsprings and suppress the markers of OS.

ROI-scavenging enzyme activities as toxicity biomarkers in three species of marine microalgae exposed to model contaminants (copper, Irgarol and atrazine).

There is a need to develop efficient tools to prevent damage to marine ecosystems due to pollution. Since microalgae play a key role in marine ecosystems, they are considered potentially useful for quick and sensitive toxicity bioassays. In this study an integrative analysis has been carried out of the anti-oxidant enzyme activities of marine microalgae species. Three marine microalgae species (Cylindrotheca closterium, a benthic diatom; Phaeodactylum tricornutum, a diatom which has been used as model organism in toxicity bioassays; and Rhodomonas salina, a cryptophyceae which is considered to present a certain level of heterotrophy) were exposed to selected concentrations of three model pollutants: copper (5 and 10µg L(-1)), atrazine (25 and 50µg L(-1)) and Irgarol (0.5 and 1.0µg L(-1)). These pollutant concentrations are environmentally relevant for coastal ecosystems, and have been selected for checking the efficiency of the reactive oxygen intermediate (ROI) scavenging enzyme system of these organisms. Superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APx) and glutathione peroxidase (GPx) activities were measured at the end of 24h exposure. The integrated biomarker response (IBR) index - in our case for oxidative stress - has been employed to evaluate the ROI-scavenging enzyme system for each species and each treatment. In general, the SOD and CAT enzyme activities measured were higher in exposed populations than in controls, whereas APx and GPx activities showed the opposite trend. These microalgae showed significant responses of oxidative stress biomarkers at environmentally relevant concentrations for the assayed pollutants and short exposure periods, conditions that most other model organisms cannot match. Therefore microalgae present clear advantages over other species for their prospective employment in an "early warning system".

Influence of Pseudomonas aeruginosa as PGPR on oxidative stress tolerance in wheat under Zn stress.

Plant Growth Promoting Rhizobacteria (PGPR), whose role is still underestimated, plays an important (or perhaps essential) role in improving plant growth. The comprehensive understanding of bacterial plant growth promoting mechanism helps to get sustainable agriculture production under biotic and abiotic stresses. In the present study, plant growth promoting (PGP) bacterial strain Pseudomonas aeruginosa having maximum inhibitory concentration of 1500mg kg(-1) against Zn was isolated from arable land, irrigated with industrial effluent and evaluated to determine it bioremediation potential. The study was mainly focused on plant biomass production, nutrient uptake and oxidative stress tolerance in relation to the activities of antioxidative enzymes and the content of non-enzymatic antioxidants. The oxidative stress tolerance was measured by estimating the MDA accumulation as well as H2O2 production in wheat plants under Zn (1000mg kg(-1)) stress and inoculation of soil with Zn resistant Pseudomonas aeruginosa. Zn in rooting medium reduced the plant growth, leaf photosynthetic pigments as well as uptake of N and P. However, content of MDA and H2O2 increased at higher concentration of Zn. Inoculation of P. aeruginosa improved the uptake of P and N in wheat plants with an increase in leaf chlorophyll, total soluble protein and plant biomass production. Analysis of plant root and shoot disclosed that Zn concentration was significantly lowered in P. aeruginosa inoculated zinc stressed plants as compare to the plants grown under Zn stress only. The amelioration of adverse effects of Zn stress on biomass production due to P. aeruginosa inoculation was related with enhanced antioxidative enzyme activities (SOD, POD and CAT), and the contents of non-enzymatic components such as ascorbic acid and total phenolics (TPC) as compare to Zn-treated plants. The up-gradation in antioxidative defense mechanism, resulted a reduction in H2O2 and MDA content due to the scavenging of ROS by antioxidants. It was concluded that P. aeruginosa is an ideal candidate for bioremediation and wheat growth promotion against Zn-induced oxidative stress by improving the availability of necessary nutrient, eliciting antioxidant defense system as well as by lowering the Zn metal uptake.

Oxidative stress status in patients with melasma.

BACKGROUND: Melasma is an acquired skin disease characterized clinically by development of gray-brown macules or patches. The lesions have geographic borders and most often seen on face and less frequently on the neck and forearms. Pathogenesis has not been completely understood yet. Although the disease constitutes a very disturbing cosmetic problem, it has not obtained an efficient treatment. There were not any studies in the literature that evaluates the role of oxidative stress in melasma. OBJECTIVES: The evaluation of the role of oxidative stress in melasma. METHODS: Fifty melasma patients and 50 healthy volunteers were included in the study. The diagnosis was made clinically and the patients were evaluated by Melasma Area Severity Index. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde, nitric oxide, protein carbonyl levels were measured both in the melasma group and the control group. RESULTS: SOD and GSH-Px enzyme activities were significantly higher in the patient group in comparison with the control group (p < 0.001). Protein carbonyl levels were significantly lower in the patient group (p < 0.001). CONCLUSION: The results show that the balance between oxidant and anti-oxidants was disrupted and the oxidative stress increased in melasma. These results improve the understanding of etiology-pathogenesis of the disease and its treatment.

Potential Effects of Garlic (Allium sativum L.) on the Performance, Immunity, Gut Health, Anti-Oxidant Status, Blood Parameters, and Intestinal Microbiota of Poultry: An Updated Comprehensive Review.

The use of antibiotics as growth promoters or for the prevention of some poultry diseases has faced global concern and serious criticism. Their addition to poultry feed has shown hazardous effects, including the development of antimicrobial resistance and a potentially harmful effect on human health. To eliminate these threats, there is increasing interest in natural alternatives. Plant derivatives such as garlic (Allium sativum L.) and its derivatives are presently extensively used in the poultry production system. The dietary supplementation of broilers and layers with garlic induced improvement in the production parameters, carcass quality, and intestinal integrity. The modulation of the immune response against some important viral diseases has resulted from the supplementation of poultry with garlic. Moreover, garlic has been shown to modulate gut health through antibacterial and antiparasitic activities. Treatment with garlic can also mitigate oxidative stress and reduce free-radical production. The reduction of cholesterol levels and improvement of some liver and blood parameters were also reported following the dietary inoculation of garlic. This review was designed to investigate the influence of garlic as a dietary additive on the performance, immunity, gut health, anti-oxidant status, blood parameters, and intestinal microbiota of poultry.

Gut microbial metalloproteins and its role in xenobiotics degradation and ROS scavenging.

The gut microbial metalloenzymes play an important role in maintaining the balance between gut microbial ecosystem, human physiologically processes and immune system. The metals coordinated into active site contribute in various detoxification and defense strategies to avoid unfavourable environment and ensure bacterial survival in human gut. Metallo-ß-lactamase is a potent degrader of antibiotics present in periplasmic space of both commensals and pathogenic bacteria. The resistance to anti-microbial agents developed in this enzyme is one of the global threats for human health. The organophosphorus eliminator, organophosphorus hydrolases have evolved over a course of time to hydrolyze toxic organophosphorus compounds and decrease its effect on human health. Further, the redox stress responders namely superoxide dismutase and catalase are key metalloenzymes in reducing both endogenous and exogenous oxidative stress. They hold a great importance for pathogens as they contribute in pathogenesis in human gut along with reduction of oxidative stress. The in-silico study on these enzymes reveals the importance of point mutation for the evolution of these enzymes in order to enhance their enzyme activity and stability. Various mutation studies were conducted to investigate the catalytic activity of these enzymes. By using the "directed evolution" method, the enzymes involved in detoxification and defense system can be engineered to produce new variants with enhance catalytic features, which may be used to predict the severity due to multi-drug resistance and degradation pattern of organophosphorus compounds in human gut.

Impact of dual neutralization of TNF-α and IL-1ß along with Gentamicin treatment on the functions of blood and splenic neutrophils and its role on improvement of S. aureus induced septic arthritis.

Researches of recent past years have emphasized potential of antibiotics to improve septic arthritis but as multi-drug resistant strains like MRSA are emerging fast, new alternative therapeutic advances are high in demand. This study aims to figure out the role of neutrophils in regulating inflammatory responses of S. aureus induced septic arthritis while using TNF-α Ab or IL-1ß Ab along with antibiotic gentamicin or both in combination. In this study, role of anti-oxidant enzymes were investigated and correlated with generated ROS level. While expression of TLR2, TNFR2, MMP2, RANKL, SAPK/JNK in the spleen were evaluated through western blot. Serum activity of IL-8, IL-10, IL-12, OPG, OPN, CRP was assessed using ELISA. Flow cytometry study evaluated inflamed neutrophil population. Results have shown TNF-α neutralization along with gentamicin was able to reduce arthritic swelling prominently. While combination therapy effectively reduced blood neutrophil ROS activity, arginase activity, MPO activity along with spleen bacterial burden. Serum OPG, CRP, IL-10 level got reduced while serum OPN, IL-8 and IL-12 level enhanced in treatment groups, showing mitigation of inflammatory damage. Overall, it is a novel work that observed how antibiotic and antibody therapy enhanced neutrophil function positively to combat sepsis. This study may not be fully applicable in clinical trials as it is performed with animal model. Clinical trials include crystalline and inflammatory arthritides, trauma, neoplasm. Interdisciplinary collaboration between radiology, orthopaedic surgery and knowledge of animal system responses may give better idea to find proper therapeutic approach in future research works.

Repurposing Diltiazem for Its Neuroprotective Anti-Dementia Role against Intra-Cerebroventricular Streptozotocin-Induced Sporadic Alzheimer's Disease-Type Rat Model.

Alzheimer's disease (AD) is an age-related neuropsychiatric disorder and a common cause of progressive dementia. Diltiazem (DTZ), the non-dihydropyridine benzothiazepine class of calcium channel blocker (CCB), used clinically in angina and other cardiovascular disorders, has proven neurological benefits. In the present study, the neuroprotective anti-dementia effects of DTZ against intra-cerebroventricular-streptozotocin (ICV-STZ)-induced sporadic AD (SAD)-type rat model was investigated. ICV-STZ-induced cognitive impairments were measured via passive avoidance and Morris water maze tasks. Anti-oxidative enzyme status, pro-inflammatory markers, and amyloid-beta (Aß) protein expression in rat brain tissues were measured using ELISA kits, Western blotting, and immunostaining techniques. The data revealed that ICV-STZ injection in rats significantly induced cognitive deficits and altered the levels of oxidative and pro-inflammatory markers (p < 0.05~p < 0.001). Treatment with DTZ (10 mg/kg, 20 mg/kg, and 40 mg/kg, p.o.) daily for twenty-one days, 1 h before a single ICV-STZ (3 mg/kg) injection, significantly improved cognitive impairments and ameliorated the ICV-STZ-induced altered nitrite, pro-inflammatory cytokines (TNF-α, and IL-1ß) and anti-oxidative enzyme levels (superoxide dismutase, lipid peroxidation, and glutathione). Further, DTZ restored the increased Aß protein expression in ICV-STZ-induced brain tissue. Considering the results obtained, DTZ might have a potential therapeutic role in treating and managing AD and related dementia pathologies due to its anti-dementia activity in SAD-type conditions in rats induced by ICV-STZ.

High-intensity interval training reduced oxidative stress and apoptosis in the hippocampus of male rats with type 2 diabetes: The role of the PGC1α-Keap1-Nrf2 signaling pathway.

Objectives: This study aimed to determine the effect of 8-week high-intensity interval training (HIIT) on oxidative stress and apoptosis in the hippocampus of male rats with type 2 diabetes (T2D). The study focused on examining the role of proliferator-activated receptor gamma co-activator 1α (PGC1α)/Kelch-like ECH-associated protein Keap1/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Materials and Methods: Twenty-eight 8-week-old Wistar rats were randomly assigned to one of four groups (n=7): control (Con), type 2 diabetes (T2D), exercise (Ex), and exercise + type 2 diabetes (Ex+T2D). The Ex and Ex+T2D groups completed an 8-week exercise program consisting of 80-100% Vmax and 4-10 intervals. The homeostasis model assessment of insulin resistance (HOMA-IR) index was used to assess insulin resistance. The levels of Bcl2, BAX, musculoaponeurotic fibrosarcoma (Maf), Nrf2, Keap1, and PGC1α in the hippocampus were assessed using the western blot method. Additionally, the levels of antioxidant enzymes in the hippocampus were measured using ELISA. Results: The findings indicated that the T2D group had lower levels of antioxidant enzymes, Maf, Bcl2, PGC1α, and Nrf2, and higher levels of BAX and Keap1 in the hippocampus. Conversely, the HIIT group exhibited increased levels of antioxidant enzymes, Maf, Bcl2, Nrf2, and PGC1α, along with decreased levels of BAX and Keap1 in the hippocampus. Conclusion: The study demonstrated that 8-week HIIT was effective in reducing hippocampal apoptosis and oxidative stress induced by T2D by activating the PGC1α-Keap1-Nrf2 signaling pathway. The metabolic changes induced by exercise may lead to an increase in PGC1 expression, which is the primary stimulator of the Keap1-Nrf2 signaling pathway.

Novel palladium(II) and Zinc(II) Schiff base complexes: Synthesis, biophysical studies, and anticancer activity investigation.

BACKGROUND: Schiff base metal complexes are considered promising chemotherapeutic agents due to their potential application in cancer therapy. METHODS: The current work sought to synthesize a brand-new Schiff base ligand obtained from 2-hydroxybenzohydrazide and (E)- 1-(2-(p-tolyl)hydrazono)propan-2-one with metal ions which included Pd(II) and Zn(II) ions. Elemental analyses, FT-IR, mass spectra, 1H NMR, UV-Vis spectrometer, and computational analysis characterized the compound's structure. In vitro, the breast cancer cell line (MCF-7) was tested for its sensitivity to Schiff base (HL) and its Pd(II) and Zn(II) complexes. The half-maximal inhibitory concentration IC50 of the compounds was determined and used to perform the comet assay, which was carried out to reveal the photo-induced DNA damaging ability of the compounds of individual cells. Moreover, the compounds' effects on antioxidant defense systems of enzymes in cells: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and oxidant Malondialdehyde (MDA) were examined in MCF-7 cells. RESULTS: The Pd(II) complex displayed approximately the same IC50 as Cisplatin, while Zn(II) complex had better activity than Cisplatin with very low IC50, 1.40 µg/ml. Significant alterations in SOD, CAT, GPx, and MDA production were discovered, inducing oxidative stress, enlarging ROS production, and reducing the antioxidant amount. This change was approximately similar in most compounds. Consequently, it promoted apoptosis, particularly the Zn(II) complex, which demonstrated an improved impact because of its ability to influence the antioxidant defense systems of enzymes, mostly SOD and GPx, besides increasing MDA levels. CONCLUSION: It can be concluded that Zn(II) complex is the most effective anticancer drug since it induced a very similar genotoxic effect as Cisplatin and has a very low IC50 value.