N-Acetylcysteine Ineffective in Alleviating Hangover from Binge Drinking: A Clinical Study.

Alcohol hangover (veisalgia) is a fairly common phenomenon. The pathogenesis of veisalgia is not understood and treatment has not yet been established. Occasionally, students take N-acetylcysteine (NAC) before binge drinking to alleviate hangover. The aim of this study was to evaluate the effect of NAC on serum levels of electrolytes, enzymes, oxidative stress biomarkers and symptoms of veisalgia in binge drinking. In this randomized, double-blind, placebo-controlled study, healthy students were randomly assigned into two groups: one receiving NAC and the other receiving a placebo. Blood samples were taken before drinking, 30 min after a 1.5 h long drinking session, and the subsequent morning. Serum levels of electrolytes, urea, enzymes, ethanol, 8-Hydroxydeoxyguanosine (8-OHdG) and N-epsilon-hexanoyl-lysine were measured. The participants completed the Acute Hangover Severity Scale (AHSS) assessment based on symptoms, and 40 students (20 male), aged 23 ± 2 years, were included in the study. Their mean blood ethanol concentration was 1.4 g/kg. Serum sodium levels were increased after drinking, and urea decreased the following morning compared to their levels before drinking in both groups. Serum 8-OHdG levels were increased after drinking and remained elevated until the following morning, compared to the levels before drinking, in both groups. NAC had no effect on sodium, urea and 8-OHdG levels or the symptoms of veisalgia. In conclusion, binge drinking causes a transient increase in serum sodium and as a prolonged increase in oxidative marker 8-OHdG levels. NAC had no effect on the sodium and 8-OHdG levels.

Ameliorative effects of sildenafil against carbon tetrachloride induced hepatic fibrosis in rat model through downregulation of osteopontin gene expression.

The liver carries out many essential tasks, such as synthesising cholesterol, controlling the body's storage of glycogen, and detoxifying metabolites, in addition to performing, and regulating homeostasis. Hepatic fibrosis is a pathological state characterized by over accumulation of extracellular matrix (ECM) including collagen fibers. Sildenafil (a selective inhibitor of type 5 phosphodiesterase) has anti-inflammatory, antioxidant and anti-apoptotic properties. It is commonly used to treat erectile dysfunction in male. The purpose of the current investigation was to evaluate sildenafil's hepatoprotective potential against liver fibrosis in rats that was caused by carbon tetrachloride (CCl4). Liver enzymes and oxidative markers as well as profibrotic genes were determined. The findings showed that sildenafil alleviates the hepatic dysfunctions caused by CCl4 by restoring normal levels of ALT, AST, and GGT as well as by restoring the antioxidant status demonstrated by increased glutathione (GSH), and catalase. In addition, a significantly down-regulated the mRNA expressions of profibrotic genes [collagen-1α, IL-1ß, osteopontin (OPN), and transforming growth factor-ß (TGF-ß)]. Additionally, sildenafil lessens the periportal fibrosis between hepatic lobules, congestion and dilatation in the central vein, and the inflammatory cell infiltrations. As a result, it is hypothesized that sildenafil may be helpful in the management of hepatotoxicity brought on by CCl4 through suppressing OPN.

Mitigation of drought stress in maize and sorghum by humic acid: differential growth and physiological responses.

BACKGROUND: Drought is a major determinant for growth and productivity of all crops, including cereals, and the drought-induced detrimental effects are anticipated to jeopardize world food security under the ongoing global warming scenario. Biostimulants such as humic acid (HA) can improve drought tolerance in many cereals, including maize and sorghum. These two plant species are genetically related; however, maize is more susceptible to drought than sorghum. The physiological and biochemical mechanisms underlying such differential responses to water shortage in the absence and presence of HA, particularly under field conditions, are not fully understood. RESULTS: Herein, the effects of priming maize and sorghum seeds in 100 mg L-1 HA on their vegetative growth and physiological responses under increased levels of drought (100%, 80%, and 60% field capacity) were simultaneously monitored in the field. In the absence of HA, drought caused 37.0 and 58.7% reductions in biomass accumulation in maize compared to 21.2 and 32.3% in sorghum under low and high drought levels, respectively. These responses were associated with differential retardation in overall growth, relative water content (RWC), photosynthetic pigments and CO2 assimilation in both plants. In contrast, drought increased root traits as well as H2O2, malondialdehyde, and electrolyte leakage in both species. HA treatment significantly improved the growth of both plant species under well-watered and drought conditions, with maize being more responsive than sorghum. HA induced a 29.2% increase in the photosynthetic assimilation rate in maize compared to 15.0% in sorghum under high drought level. The HA-promotive effects were also associated with higher total chlorophyll, stomatal conductance, RWC, sucrose, total soluble sugars, total carbohydrates, proline, and total soluble proteins. HA also reduced the drought-induced oxidative stress via induction of non-enzymic and enzymic antioxidants at significantly different extents in maize and sorghum. CONCLUSION: The current results identify significant quantitative differences in a set of critical physiological biomarkers underlying the differential responses of field-grown maize and sorghum plants against drought. They also reveal the potential of HA priming as a drought-alleviating biostimulant and as an effective approach for sustainable maize and sorghum production and possibly other crops in drought-affected lands.

The priority of mesenchymal stem cells treated with melatonin in ameliorating thyroid impairment induced by amiodarone. Thorough look on the apoptotic pathway.

Amiodarone treatment has been associated with thyroid alterations. This work was planned to consider therapeutic outcome of MSCs versus MSCs treated with melatonin in minimizing amiodarone -induced deviations in thyroid. We handed-down 50 male Wistar rats, then distributed them into 5 groups; I, II, III, IV, V; control, sham control, amiodarone treated, amiodarone and MSCs treated, and amiodarone, MSCs and melatonin treated groups respectively. Light microscopic examination; levels of T3, T4 and TSH, Oxidative/antioxidative tissue markers, immune-histochemical staining (Bcl2, BAX, iNOS) and real time PCR (IL-6 and VEGF and Caspase 3) were done. Results of group III showed degenerated follicles, decreased follicular cell count and diminished colloid. Some of the follicles were dilated with signs of inflammatory response and apoptosis. Increased collagen deposition in group III was marked. The positive immune-reactive cells of Bcl-2 was decreased and that of BAX and iNOS was increased, also T3 and T4 levels were significantly decreased, but TSH was significantly increased in group III comparing it to the group I. There were highly significant diminution in both SOD and GPx and upsurge in MDA intensities in groups III, IV when correlated to the control. In group IV and V the aforementioned values were restored. The PCR results showed significant increase in IL-6 and VEGF and Caspase 3 in group III compared to the control one, whereas, their values in groups IV and V were reestablished. It is concluded that stem cells can to a great extent ameliorate the thyroid damage induced by amiodarone.But, Adding melatonin to the stem cells culture was found to have auxiliary beneficial effect in the improving the thyroid structure and function.

Systemic and local effect of oxidative stress on recurrent aphthous stomatitis: systematic review.

Recurrent aphthous stomatitis (RAS) is a chronic and recurrent inflammatory disease of the mouth. It is characterised by the appearance of painful ulcers in the oral mucosa. RAS is believed to be a multifactorial disease with genetic predisposition, environmental factors and alterations in the immune system. Oxidative stress, caused by an imbalance between free radicals and the antioxidant system, also appears to be involved in the pathogenesis of RAS. Several risk factors, such as smoking, iron and vitamin deficiency and anxiety, may contribute to the development of the disease. Understanding the underlying mechanisms may help in the prevention and treatment of RAS. We searched PubMed, Scopus and Web of Science databases for articles on oxidative stress in patients with RAS from 2000 to 2023. Studies analysing oxidant and antioxidant levels in the blood and saliva of RAS patients and healthy controls were selected. Of 170 potentially eligible articles, 24 met the inclusion criteria: 11 studies on blood samples, 6 on salivary samples and 7 on both blood and salivary samples. Multiple oxidative and antioxidant markers were assessed in blood and saliva samples. Overall, statistically significant differences were found between RAS patients and healthy controls for most markers. In addition, increased oxidative DNA damage was observed in patients with RAS. Patients with RAS show elevated levels of oxidative stress compared to healthy controls, with a significant increase in oxidative markers and a significant decrease in antioxidant defences in saliva and blood samples.

3-Demethyl-2-geranyl-4-prenylbellidifoline, a natural xanthone with diuretic and kidney protective properties.

OBJECTIVES: The diuretic and kidney protective effect of the 3-demethyl-2-geranyl-4-prenylbellidifoline (DGP) were evaluated in rats. METHODS: The normotensive (NTR) and spontaneously hypertensive rats (SHR) received, once a day for 7 days, oral treatment with DGP (0.1 mg/kg), hydrochlorothiazide (10 mg/kg), or vehicle (10 ml/kg). Urine, blood, and kidney samples were collected for further analysis. KEY FINDINGS: The urine and Na+ elimination content were significantly higher in the groups that received DGP. Furthermore, a Ca2+-sparing action was detected in the urine of DGP-treated groups, which was consistent with the reduction in calcium oxalate crystal formation. Relevantly, the treatment did not change the parameters examined in the blood. Concerning the renal analyses, DGP treatment recovered the morphological damages of the kidney corpuscle area of SHR. In addition to the differences observed between the NTR and SHR vehicle groups, DGP augmented the amount of reduced glutathione and the activity of glutathione S-transferase GST while reducing the catalase and N-acetyl-ß-D-glucosaminidase activity and nitrite levels. CONCLUSION: Together, this study displayed the prolonged diuretic action of DGP and its natriuretic, Ca2+-sparing, and antiurolytic effects. The antioxidative and anti-inflammatory effects of DGP were evidenced in SHR kidneys, opening perspectives for further studies regarding the benefits of this xanthone.

Levodopa-induced Dyskinesia in Parkinson's Disease: Plausible Inflammatory and Oxidative Stress Biomarkers.

BACKGROUND: Pathophysiology of levodopa-induced dyskinesia (LID) remains obscure. Increased dopamine metabolism due to prolonged levodopa treatment can exacerbate oxidative damage and neuroinflammatory pathology in Parkinson's disease (PD). Association of novel peripheral markers with LID severity might provide insight into LID pathomechanisms. OBJECTIVE: We aimed to study specific peripheral blood inflammatory-oxidative markers in LID patients and investigate their association with clinical severity of LID. METHOD: Motor, non-motor and cognitive changes in PD with and without LID compared to healthy-matched controls were identified. Within the same cohort, inflammatory marker (sLAG3, TOLLIP, NLRP3 and IL-1ß) levels and antioxidant enzyme activities were determined by ELISA and spectrophotometric methods. RESULTS: LID patients showed distinctly upregulated TOLLIP, IL-1ß levels with significant diminution of antioxidant activity compared to controls. Significant negative association of cognitive markers with oxidative changes was also observed. CONCLUSION: To our understanding, this is the first study that indicates the involvement of toll-like receptor-mediated distinct and low-grade inflammatory activation in LID pathophysiology.

Neuroprotective effects of trigonelline in kainic acid-induced epilepsy: Behavioral, biochemical, and functional insights.

Trigonelline, an alkaloid found in the seeds of Trigonella foenum-graecum L. (fenugreek), has been recognized for its potential in treating various diseases. Notably, trigonelline has demonstrated a neuroprotective impact by reducing intrasynaptosomal calcium levels, inhibiting the production of reactive oxygen species (ROS), and regulating cytokines. Kainic acid, an agonist of kainic acid receptors, is utilized for inducing temporal lobe epilepsy and is a common choice for establishing kainic acid-induced status epilepticus, a widely used epileptic model. The neuroprotective effect of trigonelline in the context of kainic acid-induced epilepsy remains unexplored. This study aimed to induce epilepsy by administering kainic acid (10 mg/kg, single subcutaneous dose) and subsequently evaluate the potential anti-epileptic effect of trigonelline (100 mg/kg, intraperitoneal administration for 14 days). Ethosuccimide (ETX) (187.5 mg/kg) served as the standard drug for comparison. The anti-epileptic effect of trigonelline over a 14-day administration period was examined. Behavioral assessments, such as the Novel Object Recognition (NOR) test, Open Field Test (OFT), and Plus Maze tests, were conducted 2 h after kainic acid administration to investigate spatial and non-spatial acquisition abilities in rats. Additionally, biochemical analysis encompassing intrasynaptosomal calcium levels, LDH activity, serotonin levels, oxidative indicators, and inflammatory cytokines associated with inflammation were evaluated. Trigonelline exhibited significant behavioral improvements by reducing anxiety in open field and plus maze tests, along with an amelioration of memory impairment. Notably, trigonelline substantially lowered intrasynaptosomal calcium levels and LDH activity, indicating its neuroprotective effect by mitigating cytotoxicity and neuronal injury within the hippocampus tissue. Moreover, trigonelline demonstrated a remarkable reduction in inflammatory cytokines and oxidative stress indicators. In summary, this study underscores the potential of trigonelline as an anti-epileptic agent in the context of kainic acid-induced epilepsy. The compound exhibited beneficial effects on behavior, neuroprotection, and inflammation, shedding light on its therapeutic promise for epilepsy management.

Protective effects of lycopene against zearalenone-induced reproductive toxicity in early pregnancy through anti-inflammatory, antioxidant and anti-apoptotic effects.

Zearalenone is a mycotoxin that is widely present in feed and raw materials and can cause severe reproductive toxicity. Lycopene is a natural carotenoid with antioxidant and anti-inflammatory pharmacological effects, but the protective effects of lycopene against zearalenone-induced uterine damage have not been reported. The aim of this study was to investigate the protective effect of lycopene treatment in early pregnancy on zearalenone-induced uterine damage and pregnancy impairment and its mechanism. Reproductive toxicity was induced by consecutive gavages of zearalenone at 5 mg/kg body weight during gestational days (GDs) 0-10 and in the presence or absence of oral administration of lycopene (20 mg/kg BW). The results showed that lycopene may alleviate zearalenone-induced pathological uterine histological damage and disturbances in oestradiol (E2), follicle-stimulating hormone (FSH), progesterone (P) and luteinizing hormone (LH) secretion. Lycopene increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) production, providing protection against zearalenone-induced oxidative stress in the uterus. Additionally, lycopene significantly reduced levels of pro-inflammatory cytokines, including interleukin 1ß (IL-1ß), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), and elevated levels of the anti-inflammatory factor interleukin 10 (IL-10), inhibiting the zearalenone-induced inflammatory response. In addition, lycopene improved the homeostasis of uterine cell proliferation and death via the mitochondrial apoptosis pathway. These data provide strong evidence that lycopene can be further developed into a potential new drug for the prevention or treatment of zearalenone-induced reproductive toxicity.

Correlations of whole blood heavy metals with serum immunological and oxidative markers during the early dry period and transition period of dairy cattle.

Immunological and oxidative alterations have been reported around calving in dairy cattle. In addition, the levels of heavy metals rise in the blood around parturition, which might affect body systems. Therefore, in this Research Communication we evaluate the changes in whole blood lead (Pb), arsenic (As), and cadmium (Cd) around calving, in comparison with the beginning of the dry period, and assess the correlations of these elements with immunological factors and oxidative markers. Samples were collected from 30 clinically healthy dairy cows in the early dry period (-6 w), one week before expected calving (-1 w), and one week postpartum (+1 w). The highest concentrations of Pb, As, and Cd were observed at -1 w and all the three elements decreased after parturition leading to significantly lower As and Cd, compared to -1 w (P < 0.05). The lowest levels of tumor necrosis factor-alpha, immunoglobulin G, interleukin 4, interleukin 10 and haptoglobin were found at -1 w simultaneous with the highest measures of the heavy metals, with tumor necrosis factor-alpha being significantly lower at this time (P < 0.05). At -6 w, As concentration was significantly (P < 0.05) correlated negatively (r = -0.366) and positively (r = 0.417) with total antioxidant capacity and malondialdehyde, respectively. Furthermore, at -1 w Pb and As had significant (P < 0.05) negative correlations with interferon gamma (r = -0.502) and interleukin 4 (r = -0.483), respectively. After parturition, Pb was observed to be negatively correlated with total antioxidant capacity (r = -0.538, P < 0.05). The observed results revealed that the alterations in immunological factors and antioxidant capacity around parturition were correlated with Pb and As levels.

Effects of chromium supplementation on oxidative stress biomarkers.

Aim: This systematic review and meta-analysis aimed to evaluate the effects of chromium supplementation on oxidative stress biomarkers such as superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPX), malondialdehyde (MDA), total antioxidant status (TAS), thiobarbituric acid reactive substances (TBARS), catalase (CAT), nitric oxide (NO), total antioxidant capacity (TAC) and protein carbonyl. Methods: Relevant studies, published from inception until July 2019, were searched through PubMed/Medline, Scopus, ISI Web of Science, Embase, and Google Scholar. All randomized clinical trials investigating the effect of chromium supplementation on oxidative stress were included. Results: Out of 252 citations, 10 trials that enrolled 595 subjects were included. Chromium supplementation resulted in a significant increase in GSH (WMD: 64.79 mg/dl, 95% CI: 22.43 to 107.15; P=0.003) but no significant change in MDA, TAS, TBARS levels, SOD, CAT levels and GPX. Chromium picolinate supplementation resulted in a significant increase in TAC while failing to have a significant effect on NO. Moreover, both chromium picolinate and chromium dinicocysteinate supplementation reduced protein carbonyl levels. Conclusion: Overall, this meta-analysis demonstrated that chromium supplementation increased GSH without any significant changes in the mean of GPX, MDA, TAS, TBARS, CAT and SOD.

Canavalia ensiformis lectin induced oxidative stress mediate both toxicity and genotoxicity in Drosophila melanogaster.

Mannose/glucose-binding lectin from Canavalia ensiformis seeds (Concanavalin A - ConA) has several biological applications, such as mitogenic and antitumor activity. However, most of the mechanisms involved in the in vivo toxicity of ConA are not well known. In this study, the Drosophila melanogaster model was used to assess the toxicity and genotoxicity of different concentrations of native ConA (4.4, 17.5 and 70 µg/mL) in inhibited and denatured forms of ConA. The data show that native ConA affected: the survival, in the order of 30.6 %, and the locomotor performance of the flies; reduced cell viability to levels below 50 % (4.4 and 17.5 µg/mL); reduced nitric oxide levels; caused lipid peroxidation and increased protein and non-protein thiol content. In the Comet assay, native ConA (17.5 e 70 µg/mL) caused DNA damage higher than 50 %. In contrast, treatments with inhibited and denatured ConA did not affect oxidative stress markers and did not cause DNA damage. We believe that protein-carbohydrate interactions between ConA and carbohydrates of the plasma membrane are probably the major events involved in these activities, suggesting that native ConA activates mechanisms that induce oxidative stress and consequently DNA damage.

Antioxidant Activity of Vitamin C against LPS-Induced Septic Cardiomyopathy by Down-Regulation of Oxidative Stress and Inflammation.

In severe cases of sepsis, endotoxin-induced cardiomyopathy can cause major damage to the heart. This study was designed to see if Vitamin C (Vit C) could prevent lipopolysaccharide-induced heart damage. Eighteen Sprague Dawley male rats (n = 6) were divided into three groups. Rats received 0.5 mL saline by oral gavage in addition to a standard diet (Control group), rats received one dose of endotoxin on day 15 (lipopolysaccharide) (LPS) (6 mg/kg), which produced endotoxemia (Endotoxin group), and rats that received 500 mg/Kg BW of Vit C by oral gavage for 15 days before LPS administration (Endotoxin plus Vit C group). In all groups, blood and tissue samples were collected on day 15, six hours after LPS administration, for histopathological and biochemical analysis. The LPS injection lowered superoxide dismutase (SOD) levels and increased malondialdehyde in tissues compared with a control group. Furthermore, the endotoxin group showed elevated inflammatory biomarkers, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Both light and electron microscopy showed that the endotoxic-treated group's cardiomyocytes, intercalated disks, mitochondria, and endothelial cells were damaged. In endotoxemic rats, Vit C pretreatment significantly reduced MDA levels and restored SOD activity, minimized biomarkers of inflammation, and mitigated cardiomyocyte damage. In conclusion: Vit C protects against endotoxin-induced cardiomyopathy by inhibiting oxidative stress cytokines.

Cell-free probiotic supernatant (CFS) treatment alleviates indomethacin-induced enterocolopathy in BALB/c mice by down-modulating inflammatory response and oxidative stress: potential alternative targeted treatment.

Probiotics and their metabolites appear to be a promising approach that targets both the intestinal inflammation and dysbiosis in bowel diseases. In this context, the emergence of the probiotic cell-free supernatant (CFS) has attracted more attention as a safe and targeted alternative therapy with reduced side effects. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) can cause significant intestinal alterations and inflammation, leading to experimental enterocolopathy resembling Crohn disease. Therefore, we investigated the effect of CFS supplementation on the inflammation and the mucosal intestinal alterations induced by NSAIDs, indomethacin. In the current study, a murine model of intestinal inflammation was generated by the oral gavage (o.g) of indomethacin (10 mg/kg) to BALB/C mice. A group of mice treated with indomethacin was concomitantly treated orally by CFS for 5 days. The Body Health Condition index was monitored, and histological scores were evaluated. Moreover, oxidative and pro-inflammatory markers were assessed. Interestingly, we observed that CFS treatment attenuated the severity of the intestinal inflammation in our enterocolopathy model and resulted in the improvement of the clinical symptoms and the histopathological features. Notably, nitric oxide, tumor necrosis factor alpha, malondialdehyde, and myeloperoxidase levels were down-modulated by CFS supplementation. Concomitantly, an attenuation of NF-κB p65, iNOS, COX2 expression in the ileum and the colon was reported. Collectively, our data suggest that CFS treatment has a beneficial effect in experimental enterocolopathy model and could constitute a good therapeutic candidate for alleviating inflammatory responses and to maintain mucosal homeostasis during chronic and severe conditions of intestinal inflammation.

The effectiveness of vitamin C on quinalphos ileal toxicity: a study of histological, ultrastructural, and oxidative stress markers.

There is a significant hazard of human exposure to the organophosphates which is a constant threat, and they are responsible for numerous cases of poisoning and mammalian toxicity annually in non-target wildlife. The antioxidants, including the vitamin C (Vit C), have a protective effect on some organophosphorus compounds-induced organ damage. Quinalphos (QP) is one of these compounds. The investigation's objective is to see if there was any effect of QP on the rat ileum which could be rectified by using Vit C. Three groups of 24 animals were created. As a control, the first group was given pure water. Second group subjected to oral gavages of QPs. Third group rats were given oral gavages of Vit C plus QPs for 10 days. The reaction of ileal enterocytes to food-borne QPs was marked by poorly organized microvilli, numerous vacuoles within them, disrupted nuclei with chromatin margination, disoriented mitochondria, and an expanded intercellular space. The absorptive columnar cell illustrated many vacuoles inside with herniation of microvilli, and normal goblet cells were also seen. Many Paneth cells towards the lumen of intestinal gland contained secretory granules of different sizes and shapes. The histological architecture of the ileal mucosa in the QP plus Vit C group was found to be close to those of healthy controls. The outcomes of this study suggest that administering Vit C in rats treated with QPs protects them from ill dysfunction caused by QP.

Oxidative damage in Nile tilapia, Oreochromis niloticus, is mainly induced by water temperature variation rather than Aurantiochytrium sp. meal dietary supplementation.

We investigated whether dietary supplementation with Aurantiochytrium sp. meal, a DHA-rich source (docosahexaenoic acid, 22: 6 n-3), fed during long-term exposure to cold-suboptimal temperature (22 °C, P1), followed by short-term exposure to higher temperatures (28 °C, P2, and 33 °C, P3), would promote oxidative damage in Nile tilapia (Oreochromis niloticus). Two supplementation levels were tested: 1.0 g 100 g-1 (D1) and 4.0 g 100 g-1 (D4). A control diet, without the additive (D0, 0 g 100 g-1), and a positive control diet supplemented with cod liver oil (CLO) were also tested. The concentrations of DHA and total n-3 PUFAs in the CLO diet were similar to those found in diets D1 and D4, respectively. The parameters analyzed included hemoglobin (Hb), the antioxidant enzymes catalase, glutathione peroxidase, total glutathione, non-protein thiols, and the oxidative markers protein carbonyl and erythrocyte DNA damage. Nile tilapia did not present differences in Hb content, regardless of diet composition, but the temperature increase (P1 to P2) led to a higher Hb content. Likewise, the temperature increases promoted alterations in all antioxidant enzymes. The dietary supplementation with 1.0 g 100 g-1 Aurantiochytrium sp. meal after P1 caused minor DNA damage in Nile tilapia, demonstrating that the additive can safely be included in winter diets, despite its high DHA concentration.

Alterations of serum and saliva oxidative markers in patients with bronchial asthma.

BACKGROUNDS: The development of asthma is highly affected by exposure to exogenous and endogenous oxidative molecules, but the impact of this exposure on the pathophysiology of asthma has received little attention. OBJECTIVES: Evaluating group of selective oxidative stress markers as a tool in the management of asthma disease. METHODS: In comparison with matched healthy controls, levels of the oxidant and antioxidant markers: lipid peroxidation malondialdehyde (MDA), Total glutathione (tGSH), Uric acid (UA), Glutathione peroxidase (GPx), Catalase (CAT) superoxide dismutase (SOD), and Total antioxidant capacity (TAC) were assessed in serum and saliva of different asthma groups. RESULTS: All oxidative markers in serum and saliva of asthma patients showed significant alterations from normal healthy controls (P < 0.05), except the salivary SOD (P = 0.441). Their levels in serum were significantly correlated with asthma severity (P < 0.05), and the distinguishing between childhood and adult asthma was significantly accomplished by GPx, SOD, TAC markers (P < 0.05). However, in patients with childhood asthma no significant differences were detected between the levels of GPx, CAT, UA, MDA in serum and saliva samples (P > 0.05). CONCLUSION: Determination of the oxidative markers GPx, CAT, UA in serum or saliva can distinguish asthma from healthy states. The serum levels of UA and TAC are highly effective in monitoring asthma severity, while the salivary GPx, CAT, UA, MDA are beneficial in the management of childhood asthma. Discrimination of the age factor between asthma groups can be achieved by testing GPx, SOD, TAC in serum.

The Effects of Probiotic Supplementation on Clinical Symptom, Weight Loss, Glycemic Control, Lipid and Hormonal Profiles, Biomarkers of Inflammation, and Oxidative Stress in Women with Polycystic Ovary Syndrome: a Systematic Review and Meta-analysis of Randomized Controlled Trials.

The purpose of this systematic review and meta-analysis of randomized controlled trials (RCTs) is to determine the effectiveness of probiotic supplementation on clinical symptoms, weight loss, glycemic control, lipid and hormonal profiles, and biomarkers of inflammation and oxidative stress in women with polycystic ovary syndrome (PCOS). Eligible studies were systematically searched from Cochrane Library, Embase, Medline, and Web of Science databases until January 2019. Cochran (Q) and I-square statistics were used to measure heterogeneity among included studies. Data were pooled by using random-effect model and expressed as standardized mean difference (SMD) with 95% confidence interval (CI). Eleven articles were included in this meta-analysis. Probiotic supplementation significantly decreased weight (SMD - 0.30; 95% CI, - 0.53, - 0.07; P = 0.01), body mass index (BMI) (SMD - 0.29; 95% CI, - 0.54, - 0.03; P = 0.02), fasting plasma glucose (FPG) (SMD - 0.26; 95% CI, - 0.45, - 0.07; P < 0.001), insulin (SMD - 0.52; 95% CI, - 0.81, - 0.24; P < 0.001), homeostatic model assessment for insulin resistance (HOMA-IR) (SMD - 0.53; 95% CI, - 0.79, - 0.26; P < 0.001), triglycerides (SMD - 0.69; 95% CI, - 0.99, - 0.39; P < 0.001), VLDL-cholesterol (SMD - 0.69; 95% CI, - 0.99, - 0.39; P < 0.001), C-reactive protein (CRP) (SMD - 1.26; 95% CI, - 2.14, - 0.37; P < 0.001), malondialdehyde (MDA) (SMD - 0.90; 95% CI, - 1.16, - 0.63; P < 0.001), hirsutism (SMD - 0.58; 95% CI, - 1.01, - 0.16; P < 0.001), and total testosterone levels (SMD - 0.58; 95% CI, - 0.82, - 0.34; P < 0.001), and also increased the quantitative insulin sensitivity check index (QUICKI) (SMD 0.41; 95% CI, 0.11, 0.70; P < 0.01), nitric oxide (NO) (SMD 0.33; 95% CI 0.08, 0.59; P = 0.01), total antioxidant capacity (TAC) (SMD 0.64; 95% CI, 0.38, 0.90; P < 0.001), glutathione (GSH) (SMD 0.26; 95% CI, 0.01, 0.52; P = 0.04), and sex hormone binding globulin (SHBG) levels (SMD 0.46; 95% CI, 0.08, 0.85; P = 0.01). Probiotic supplementation may result in an improvement in weight, BMI, FPG, insulin, HOMA-IR, triglycerides, VLDL-cholesterol, CRP, MDA, hirsutism, total testosterone, QUICKI, NO, TAC, GSH, and SHBG but did not affect dehydroepiandrosterone sulfate levels, and total, LDL, and HDL cholesterol levels in patients with PCOS.

Effect of combined G6PD deficiency and diabetes on protein oxidation and lipid peroxidation.

BACKGROUND: Oxidative Stress, an imbalance in the pro-oxidant/antioxidant homeostasis, occurs in many physiological and non-physiological processes and several human diseases, including diabetes mellitus (DM) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Since the incidence of G6PD deficiency in Jordan and many parts of the world is high, this study aimed to measure the effect of G6PD deficiency on the oxidative markers and the antioxidant glutathione (GSH) in diabetic and non-diabetic individuals. METHODS: Whole blood G6PD deficiency was screened by the fluorescent spot method, and erythrocyte G6PD activity was determined using a quantitative assay. Since protein carbonyl (PC) and malondialdehyde (MDA) are the most widely measured markers for protein and lipid oxidation, respectively, plasma PC and MDA, in addition to blood GSH were determined by spectrophotometric assays, as biomarkers of oxidative stress. RESULTS: The incidence of G6PD deficiency among the diabetic subjects was 15%. PC level in patients with diabetes and in G6PD-deficient subjects was 5.5 to 6-fold higher than in non-diabetic subjects with sufficient G6PD levels (p<0.001). This fold increase was doubled in diabetic patients with G6PD deficiency (p<0.001). Furthermore, the MDA level was significantly increased by 28-41% in G6PD-deficient, diabetics with sufficient G6PD, and diabetics with G6PD deficiency compared to MDA level in non-diabetic with sufficient G6PD. On the other hand, GSH was significantly reduced to half in G6PD-deficient subjects and in diabetics with G6PD-deficiency. CONCLUSIONS: The results showed that diabetes and G6PD deficiency increased protein oxidation and lipid peroxidation. However, the combination of both disorders has an additive effect only on protein oxidation. On the other hand, GSH level is only reduced in G6PD deficiency. In addition, diabetes and G6PD deficiency appear to be genetically linked since the incidence of G6PD deficiency among people with diabetes is more than the general population.

Effects of ginger supplementation on biomarkers of oxidative stress: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: The present systematic review and meta-analysis were conducted to investigate the effects of ginger on biomarkers of oxidative stress such as glutathione peroxidase (GPx), malondialdehyde (MDA), and total antioxidant capacity (TAC) this meta-analysis was performed. METHODS: Five databases were searched from inception to May 2020 using relevant keywords. Results were reported as bias-corrected standardized mean difference (Hedges' g) with 95 % confidence intervals (CI) using random-effects models. RESULTS: Eleven RCTs were included. Ginger resulted in significantly increased on GPx (Hedges' g: 1.93, 95 % CI: 0.20 to 3.66, P = 0.029) and significant reduction in MDA (Hedges' g: -1.45, 95 % CI: -2.31 to -0.59, P = 0.001), but no significant change in TAC (Hedges' g: 0.42, 95 % CI: -0.03 to 0.88, P = 0.069). Greater reduction in MDA was detected in trials using ≤1 g ginger, lasted <12 weeks, participants aged ≥30 years old, among both gender and were conducted sample size ≤40. TAC was increased by administered high doses of ginger, lasted ≥12 weeks, mean age ≥30, sample size >40, and both gender and female. CONCLUSION: Overall, this meta-analysis demonstrated ginger supplementation decreased MDA and increased GPx but the results showed no significant alterations in TAC activities.