Carbonyl Levels Research Articles

Redox biomarker levels in patients with myelodysplastic syndrome.

Myelodysplastic syndrome (MDS) is a heterogeneous clonal disorder characterized by insufficient hematopoiesis, peripheral blood cytopenia and an increased risk for malignant transformation to acute myeloid leukemia. Several factors, such as age, sex and lifestyle, promote the development of MDS syndrome. Oxidative stress, along with its detrimental effects, cause hematological disorders; however, its role in the pathogenesis of MDS is unknown. The present study enrolled 50 patients with MDS and 50 additional healthy individuals to assess the endogenous antioxidant defense system by measuring specific redox biomarkers at the time of diagnosis. Glutathione (GSH) levels, catalase (CAT) activity and total antioxidant capacity (TAC) were measured in red blood cells, whereas levels of thiobarbituric acid reactive substances (TBARS) and protein carbonyls were measured in the plasma. A decrease in GSH levels, increased TBARS levels and TAC levels were observed in patients with MDS compared with healthy volunteers, supporting the hypothesis that oxidative stress disturbance could promote MDS.

The supply of branched-chain amino acids and branched-chain keto acids alter lipid metabolism, oxidative stress, and apoptosis in primary bovine hepatocytes.

Fatty liver impairs liver function and reduces productivity in dairy cows. Our previous in vivo findings demonstrated that branched-chain amino acids (BCAA) or branched-chain ketoacid (BCKA) improved liver function and lactation performance in dairy cows; however, the underlying mechanisms remain unclear. This study aimed to assess the impact of BCAA or BCKA supplementation on intracellular triglyceride (TG) accumulation, lipid metabolism, antioxidant response, and apoptosis in hepatocytes. Treatments were: control (CON): customized medium with amino acids, volatile fatty acids, fatty acids (FA), glucose, choline, insulin, and albumin concentrations equal to circulating levels in cows 4d postpartum; BCAA: CON + 33% additional BCAA of plasma BCAA 4d postpartum; and BCKA: CON + 33% additional BCKA of plasma BCAA 4d postpartum. Compared to CON, BCAA and BCKA reduced intracellular TG concentration by 32% and 40%, respectively, after 72 h. BCAA and BCKA enhanced the uptake of palmitic acid, but upregulated the expression of genes regulating FA oxidation. Although mitochondrial membrane potential was reduced, oxidative protein damage (protein carbonyl levels) was decreased in BCAA- and BCKA-treated hepatocytes without changes in mitochondrial copy number. Additionally, compared to CON, BCAA and BCKA decreased the expression of executioner caspases (caspase 3 and caspase 7) and reduced the portion of hepatocytes with activated caspase 3/7, suggesting reduced apoptosis. These findings suggest that BCAA or BCKA supplementation improves hepatocyte lipid metabolism, antioxidant defenses, and apoptosis regulation, potentially mitigating the adverse effects of fatty liver. These mechanisms likely underlie the previously observed improvements in liver function and lactation performance.

Riboflavin-mediated ultraviolet photosensitive oxidation of beef myofibrillar proteins with different storage times.

The study was designed to investigate the mechanism of Riboflavin (RF)-mediated UVA photosensitive oxidation on beef myofibrillar proteins (MP) oxidized at different storage times. To elucidate the direct relationship between RF and protein oxidation, the mechanism of action was analyzed in terms of amino acid and side chain residues, protein structure, and protein oxidative metabolism. Oxidation of MP resulted in significant changes in the levels of carbonyls, sulfhydryls, Lysine, Arginine, Threonin, and Histidine. The oxidized MP secondary structure was changed, fluorescence intensity decreased, and surface hydrophobicity increased. Metabolomics results revealed that RF-mediated UVA photosensitized oxidation is primarily mediated by Riboflavin metabolism and co-regulated with Phenylalanine metabolism. Moreover, with the increase of frozen storage time, Arginine and proline metabolism was inhibited, and the contents of creatine were significantly reduced, which exacerbated MP oxidative damage. The results provide a theoretical basis for unraveling the mechanism of RF-mediated UVA photosensitive oxidation of MP.

Chalcogen dihydrobenzofuran compounds as potential neuroprotective agents: an in vitro and in silico biological investigation.

Oxidative stress arises from an imbalance between reactive species (RS) production and the antioxidant defense, increasing the brain susceptibility to neurodegenerative and psychiatric diseases. Besides, changes in the expression or activity of neurotransmitter metabolism enzymes, such as monoamine oxidases (MAO), are also associated with mental disorders, including depression. Considering this, antioxidant and MAO-A activity inhibitory potential of six 2,3-chalcogenodihydrobenzofurans (2,3-DHBF) was investigated through in vitro and in silico tests. Compounds 1 to 5 incorporate sulfur (S) as chalcogen, whereas compound 6 integrates tellurium (Te). A screening (compounds 1-6) of cerebral MAO-A activity showed inhibitory activity for the compounds 2, 4, 5, and 6. Among sulfur compounds, compound 2 demonstrated superior scores in docking studies, yielding a value of - 9.9 kcal/mol. Selected for concentration-response curves, compounds 2 (with S) and 6 (with Te) inhibited MAO-A at concentrations equal to or higher than 25 μM. In a redox screening test, only compound 6 showed antioxidant effects. Concentration-response curves indicated that compound 6 reduced lipid peroxidation and protein carbonylation levels in mouse brain tissue (≥ 0.5 μM), as well as reduced RS levels (≥ 1 μM). Furthermore, the compound 6 (≥ 5 μM) was effective in reducing the ferric ion (FRAP). In radical scavenging tests such as 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS), compound 6 showed significant results in concentrations from 50 μM and mimicked the enzyme glutathione S-transferase (GST) at 100 μM. In summary, this study demonstrated the cerebral antioxidant and/or MAO-A inhibition properties of 2,3-DHBF, presenting potential as neuroprotective candidates.

Stranded heavy fuel oil exposure causes deformities, cardiac dysfunction, and oxidative stress in marine medaka Oryzias melastigma using an oiled-gravel-column system.

Heavy fuel oil (HFO) stranded on the coastline poses a potential threat to the health of marine fish after an oil spill. In this study, an oiled-gravel-column (OGC) system was established to investigate the toxic effects of stranded HFO on marine medaka Oryzias melastigma. HFO 380# (sulfur content 2.9%) was chosen as one type of high sulfur fuel oil for acute toxicity tests. The marine medaka larvae were exposed to the OGC system effluents with oil loading rates of 0 (control), 400, 800, 1600, and 3200µg HFO/g gravel for 144h, respectively. Results showed that a prevalence of blue sac disease signs presented teratogenic effects, including decreased circulation, ventricular stretch, cardiac hemorrhage, and pericardial edema. Moreover, the treatments (800, 1600, and 3200µg oil/g gravel) induced severe cardiotoxicity, characterized by significant bradycardia and reduced stroke volume with an overt decrease in cardiac output. Additionally, the antioxidant enzyme activities, including catalase (CAT), peroxidase (POD), and glutathione S-transferase (GST) were significantly upregulated at 800-3200µg oil/g gravel except for a marked inhibition of CAT activity at 3200µg oil/g gravel. Furthermore, significantly elevated protein carbonyl (PCO) levels were detected, suggesting that the organisms suffered severe protein oxidative damage subjected to the exposure. Overall, stranded HFO 380# exposure activated the antioxidant defense system (up-regulated POD and GST activities) of marine medaka and disrupted CAT activity, which could result in an oxidative stress state (elevated PCO levels) and might further contribute to cardiac dysfunction, deformities, and mortality.

A Moderate Intake of Beer Improves Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in a High-Fat Diet (HFD)-Induced Mouse Model.

Beer and its components show potential for reducing hepatic steatosis in rodent models through multiple mechanisms. This study aimed to evaluate beer's anti-steatotic effects in a high-fat diet (HFD)-induced mouse model of Metabolic dysfunction-Associated Liver Disease (MASLD) and to explore the underlying mechanisms. In the HFD group, steatosis was confirmed by altered blood parameters, weight gain, elevated liver lipid content, and histological changes. These markers were normalized in the HFD+beer group, reaching levels similar to the control (CTR) group. Protein carbonylation and lipid peroxidation levels were consistent across all groups, suggesting that the model represents an early stage of MASLD without oxidative stress. Transcriptomic and CpG methylation analyses revealed clear distinctions between the CTR and HFD groups. RNA sequencing identified 162 differentially expressed genes (DEGs) between the CTR and HFD groups, primarily related to inflammation and lipid regulation. Beer consumption modified the health of the HFD mice, affecting inflammation but not lipid homeostasis (CTR vs. HFD+beer, DEGs = 43). The CpG methylation analysis indicated that beer lowered methylation, impacting genes linked to lipid accumulation and inflammation. A cecal metabolite analysis suggested that beer improved short-chain fatty acid metabolism (SCFA). In summary, a moderate beer intake may mitigate MASLD by modulating lipid metabolism and SCFA pathways, likely through polyphenol activity.

Protective effects of ghrelin on pancreas in fructose diet and streptozotocin-induced diabetic rats.

Ghrelin, which is widely expressed in central and peripheral tissues, has several metabolic effects. It has been suggested that these effects may include anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Therefore, we aimed to investigate the effects of ghrelin administered to diabetic rats on DNA repair and apoptosis mechanisms, and differences in oxidative stress (OS) and pancreatic hormone levels in the pancreas. Twenty-one rats were randomly divided into three groups: control, type 2 diabetes mellitus (T2DM), and T2DM treated with ghrelin (T2DM + ghrelin). We examined PCNA and PARP-1 to evaluate the effect of ghrelin on DNA repair, caspase-3 and caspase-9 to evaluate its effect on apoptosis, and insulin and glucagon to evaluate its role in regulating glucose homeostasis by immunohistochemistry in diabetic rats. Malondialdehyde, glutathione, and protein carbonyl levels, as well as catalase, glutathione-S-transferase, and superoxide dismutase (SOD) activities, were measured spectrophotometrically to detect the ghrelin effect on OS. Homeostasis model assessment for insulin resistance (HOMA-IR) and pancreatic insulin levels were assessed by ELISA method. Ghrelin may be a potential regulator of apoptosis as it significantly reduced the number of caspase-3 and caspase-9 immunopositive cells (p < 0.0001). In addition, ghrelin treatment reduced OS by decreasing glutathione (p < 0.001), malondialdehyde, and protein carbonyl, as well as the activity of SOD (p < 0.05) in diabetic rats. The results suggest that ghrelin is a potential apoptotic regulator and may be considered as a therapeutic agent due to its significant ability to suppress OS in T2DM.

The possible antioxidative effects of ketogenic diet by modifying brain klotho expression: a rat model study

ABSTRACT Objectives: The ketogenic diet (KD) has long been used as an alternative nonpharmacological therapy to manage pharmacoresistant epilepsy. The anticonvulsant mechanisms of KD have yet to be fully elucidated. The present study explored whether a KD could exert antioxidative effects by altering brain Klotho (Kl) gene expression. Methods: Thirty male rats were divided into three groups: the normal diet (ND) group received standard rat chow; the calorie-restricted diet (CRD) group was maintained at 90% of the calculated energy need; and the KD group received a diet composed of 8% protein, 2% carbohydrates, and 90% fat (per calorie macronutrient). The levels of β-hydroxybutyrate (BHB) in the serum, Kl gene expression in the brain, and Kl protein, malondialdehyde (MDA), and protein carbonyl (PC) levels in the serum and brain were evaluated by standard methods. Results: The serum BHB levels in the KD group were significantly greater than those in the ND and CRD groups (p < 0.001). The Kl expression in the brain was significantly greater in the KD group than in the ND group (p = 0.028). The brain MDA levels in the KD group were significantly lower than those in the ND group (p = 0.006). Elevated BHB was positively correlated with brain Kl expression (r = 0.668, p < 0.001). The brain MDA levels were negatively correlated with brain Kl expression (r = −0.531, p = 0.003) and serum BHB levels (r = 0.472, p = 0.020). Discussion: KD might exert antioxidative effects by increasing BHB and upregulating Kl in the brain. This could be considered a possible anticonvulsant mechanism of KD.

LncRNAs Involved in Antioxidant Response Regulation as Biomarkers of Gestational Diabetes: A Study on H19, MALAT1 and MEG3.

Recent findings highlighted the potential of long non-coding RNAs (lncRNAs) as novel indicators of gestational diabetes mellitus (GDM), as they demonstrate altered expression in metabolic disorders, oxidative stress (OS) and inflammation (IFM). The aim of this study was to evaluate the diagnostic potential and prognostic significance of the OS/IFM-related lncRNAs H19, MALAT1 and MEG3 in GDM and their correlations with redox status-related parameters. The relative quantification of selected lncRNAs from peripheral blood mononuclear cells (PBMCs) of GDM patients and controls (n = 50 each) was performed by qPCR. The expression levels were tested for correlations with metal ion concentrations, NRF2 expression, activities of glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), serum thiol content, protein carbonyl level and thiobarbituric acid reactive substances. MALAT1 and H19 were significantly downregulated in GDM patients (p = 0.0095 and p = 0.012, respectively). A correlation was observed between H19 expression and zinc levels in both GDM patients and controls. MALAT1 expression positively correlated with NFE2L2 levels in GDM patients (p = 0.026), while H19 exhibited a positive correlation with GR activity in controls (p = 0.018) and an inverse correlation with SOD activity (p = 0.048). Our data show the disturbance of OS/IFM-lncRNAs in GDM pathogenesis and illustrate the biomarker potential of the analyzed lncRNAs, as well as of certain redox status parameters.

Evaluating the efficacy of citrus fruit peel extract in preserving the quality of silver carp (Hypophthalmichthys molitrix) surimi during frozen storage

This research investigated the effects of mosambi peel extract (MPE) on the stability of proteins and textural characteristics of silver carp surimi during frozen storage at -20°C. The findings revealed that surimi fortified with 0.75% MPE displayed upgraded protein solubility (PS), water holding capacity (WHC), Ca2+-ATPase activity, and sulfhydryl (SH) content. It also exhibited reduced levels of total carbonyls and surface hydrophobicity, along with higher overall acceptability compared to surimi treated with synthetic cryoprotectants (control) throughout storage. Additionally, MPE slowed down the increase in total volatile basic nitrogen (TVBN) and protein degradation index (PI), as evidenced by SDS-PAGE showing higher intensities of myosin heavy chain (MHC) and actin over the storage period. Moreover, the incorporation of MPE effectively mitigated lipid oxidation as peroxide value (PV), and thiobarbituric acid (TBA) were lesser than control. Fourier-transform infrared spectroscopy (FTIR) peaks specified that the relative content of α-helix and β-sheet structures remained more stable in the MPE-treated group compared to the control, along with the improved gel and textural properties of surimi. Hence, this study suggests that 0.75% MPE could serve as a natural alternative to synthetic cryoprotectants, ensuring the oxidative stability of silver carp surimi during frozen storage while enriching it with beneficial bioactive compounds.

Storage causes protein oxidation of soybean meal and affects antioxidant status, digestive performance and meat quality of broilers.

This study investigated the protein oxidation of soybean meal (SBM) stored in a warehouse and the effects of SBM on growth performance, antioxidant status, digestive performance, intestinal morphology, and breast muscle quality of broilers. In total, 160 one-day-old Arbor Acres Plus broilers (half male and half female) were randomly divided into two groups with ten replicates of eight birds each: The control group was served with a basal diet including SBM stored at -20°C (FSBM), and the experimental group was served with a basal diet including SBM stored in a warehouse at room temperature for 45 days (RSBM). Compared with FSBM, the protein carbonyl level in RSBM was increased, the free and total thiol levels and in vitro digestibility of protein were decreased. The RSBM decreased the serum glutathione (GSH) level and the hepatic total superoxide dismutase (T-SOD) activity at days 21 and 42 when compared with FSBM. Further, RSBM reduced the duodenal T-SOD activity, jejunal catalase (CAT), and T-SOD activities at day 21, and decreased the duodenal CAT and T-SOD activities, jejunal T-SOD activity, and ileal GSH level and T-SOD activity at days 21 and 42 when compared with FSBM. Besides, the trypsin activity and the ratio of villus height to crypt depth in small intestines of broilers at days 21 and 42 were reduced when fed with a RSBM-contained diet. Compared with FSBM, the 24-h drip loss, shear force, and 24- and 48-h cooking loss of breast muscle were increased of RSBM group, the opposite result was observed for muscle lightness at 48 h. Room temperature storage for 45 days led a protein oxidation and decreased in vitro digestibility in SBM, and fed RSBM impaired growth performance, antioxidant status, and meat quality, reduced trypsin activity, and affected the small intestine morphology in broilers.

Ayahuasca Pretreatment Prevents Sepsis-Induced Anxiety-Like Behavior, Neuroinflammation, and Oxidative Stress, and Increases Brain-Derived Neurotrophic Factor.

The psychoactive decoction Ayahuasca (AYA) used for therapeutic and religious purposes by indigenous groups and peoples from Amazonian regions produces anti-inflammatory and neuroprotective effects. Thus, it may be useful to attenuate the neuroinflammation and related anxiety- and depressive-like symptoms elicited by inflammatory insults such as sepsis. Rats were pretreated for 3days with different doses of AYA. Twenty-four hours after, cecal ligation and puncture (CLP) was performed. On days 1-4, post-CLP behavioral tests to assess anxiety-like behavior were performed. After 24-h, neuroinflammation, oxidative stress, myeloperoxidase activity, and mitochondrial metabolism were assessed in the prefrontal cortex (PFC), hippocampus (HP), and cortex. AYA pretreatment increased the time spent in the open arms of the elevated plus maze and prevented the sepsis-induced hyper-grooming and -rearing behavior, suggesting an anxiolytic effect. AYA pretreatment increased the levels of the anti-inflammatory interleukin 4, in the PFC and the cortex, and brain-derived neurotrophic factor in the cortex. Moreover, AYA pretreatment increased myeloperoxidase activity in the PFC and the HP and decreased nitrite/nitrate concentration in the PFC, HP, and cortex of septic rats, suggesting enhanced neutrophil activation and decreased nitric oxide signaling. Furthermore, AYA pretreatment prevented lipid peroxidation in the PFC, HP, and cortex of septic rats as measured by decreased levels of thiobarbituric acid reactive substances. Levels of protein carbonyls and activity of superoxide dismutase, citrate synthase, succinate dehydrogenase, and mitochondrial respiratory chain were not affected. Together,AYA represents a promising approach to prevent sepsis-induced neuroinflammatory and oxidative stress and associated anxiety-like symptoms.

Dual intervention of Boeravinone B and Chebulinic Acid mitigates BHT-Induced toxicity in HepG2 cells: modulating apoptosis and autophagy

Butylated Hydroxytoluene (BHT) is found to exert cellular toxicity through induction of oxidative stress although being used as antioxidant in many food products. This study investigates the protective effects of two herbal compounds Boeravinone B (BB) and Chebulinic acid (CA) in combination (B4C3 i.e. BB 4 µg/mL and CA 3 µg/mL). Key findings revealed that BHT exerted toxicity through induction of ROS (234.47 a.u.) and RNS (0.042 µM/mL), but B4C3 has significantly reduced it (115.46 a.u. and 0.018 µM/mL respecctively). BHT exposure raised the activities of antioxidant enzymes such as SOD (70.9%), CAT (7.08 units/mL), GPX (1.21 units/mL), levels of protein carbonyls (3.52 units/mg) and lipid peroxides (418.34%). Whereas treatment with B4C3 decreased the levels of SOD (29.92%), CAT (3.12 units/mL), GPX (0.36 units/mL), protein carbonyls (0.91 units/mg of protein) and lipid peroxides (106.67%) during BHT exposure. It was found that 20.56% cells were apoptotic while 73.83% were autophagic during BHT treatment. However, proposed phytotherapy rescued the cells from apoptotic and autophagic death and supported cell growth which was confirmed by RT-PCR and growth analysis. Collectively, B4C3 offered a significant protection against BHT-induced cellular damage, suggesting its potential as therapeutic agents for oxidative stress-related hepatotoxicity.

Metabolic and stress resistance effects in Macrobrachium rosenbergii juveniles supplemented with Curcuma longa extract.

This work studied the effects of C. longa extract as a dietary supplement for Macrobrachium rosenbergii. Shrimp juvenile (n = 960, initial average weight 0.06 ± 0.042g and initial stocking density 0.4 animals/L) received diets with different concentrations of turmeric extract (0.05, 0.2, 1%) for 60 days, and zootechnical (weight gain, specific growth rate, initial and final condition factor) and metabolic (activities of digestive enzymes, amino acid metabolism enzymes, and energy metabolism enzymes) parameters were evaluated. A transport simulation (TS) test was conducted and, in challenged animals, survival and antioxidant status were studied. Phenolic compound content and in vitro antioxidant potential of the turmeric extract were evaluated. Turmeric extract (0.05%) significantly increased weight gain and the activity of digestive enzymes. An increase in citrate synthase activity for all concentrations of turmeric was also observed. The glutamate dehydrogenase activity in the 0.05% group was also increased by turmeric extract. The in vitro antioxidant activity of the turmeric extract was like butylated hydroxytoluene (BHT), a common antioxidant, and the total phenolic content was 0.98 ± 0.02 mmolAG/g. In animals from the TS test, turmeric extract promoted a dose-dependent increase in animal survival. Furthermore, turmeric supplementation increased the activity of the enzymes catalase, glutathione reductase, glutathione peroxidase, glutathione S-transferase, and it reduced glutathione (GSH) content. A reduction in the levels of lipid peroxidation (TBARS) and protein carbonyl was also observed in the hepatopancreas of all experimental groups. The addition of low concentrations of turmeric extract to the diet of M. rosenbergii juvenile presents great potential for application in commercial shrimp farming, since the extract (at concentrations as low as 0.05 to 1%) increased weight gain and improved the physiological and metabolic conditions of the animals, improving the use of nutrients and consequently the animals' responses to stressful conditions, such as transport.

Jerked beef as an ultraprocessed convenience food: Desalting strategies to minimize the impact on lipid and protein oxidation.

Jerked beef (JB) is a high-protein convenience food but shows high degree of oxidation owing to its severe ultraprocessing. This study aimed to investigate the effect of desalting processes on oxidative stability of JB. JB were submitted to five desalting procedures: immersion in water at room temperature for 12h without changing the water (AT12); immersion in water at room temperature for 12h followed by boiling for 30min and changing the water between the two procedures (AT12+C30); immersion in boiled water for 10, 20, and 30min (C10, C20, and C30, respectively). The desalted JB samples were refrigerated (vacuum packed and stored at 1±1°C) and analyzed at 0 and 60 days. The samples without desalting were used as a control group. AT12 samples had the lowest lipid oxidation (0.05 and 0.07mg of MDAkg-1, at T60 and T0, respectively). AT12+C30 had the lowest NaCl content (2.8 and 3.3g100g-1, at T0 and T60, respectively). C10, C20, and C30 showed a lower level of total carbonyls (p<0.05) (0.04-0.13nmolmg-1 protein), compared to control (0.53-0.93nmolmg-1 protein in T0 and T60, respectively). Only boiled, desalted meats showed the volatile compound benzaldehyde. Higher concentration of monounsaturated, polyunsaturated, and total unsaturated fatty acids in JB desalted only in boiling water (C10, C20, and C30), compared to control (p<0.05). AT12 is the best process to use, with regards to lipid oxidative stability, hardness, and NaCl content. Therefore, we conclude that it is possible to offer commercially desalted JB, as a convenience ultraprocessed product. PRACTICAL APPLICATION: Lipid oxidation is accelerated when desalting jerked beef (JB) with boiling water. Desalted JB in boiling water had detectable concentrations of benzaldehyde. •Desalting in water at 25°C/12h resulted in JB with better oxidative stability.

The Protective Effects of Citrulline on Testicular Injury Induced by Torsion and Detorsion in Adult Male Rats: An Experimental Study.

Testicular torsion is a critical urological emergency that can lead to testicular ischemia and significant tissue damage. Citrulline, a supplement known for enhancing cellular metabolism and mitigating oxidative stress and inflammation, has been explored for its protective effects against testicular injury resulting from torsion and detorsion in rat models. This study involved 42 Wistar rats, divided into six groups: Sham, torsion/detorsion (T/D), and four groups receiving varying doses of Citrulline (300, 600, 900 mg/kg) and vitamin E (20 mg/kg). A surgical procedure was performed to induce torsion by rotating the left testicle for 4 hr, followed by reperfusion. Daily oral administration of the supplements continued for one week post-surgery. Assessments included oxidative stress markers, apoptosis, inflammation, pathology, and sperm parameters. Statistical analysis was conducted using GraphPad Prism. Citrulline administration at doses of 600 and 900 mg/kg significantly reduced malondialdehyde (MDA) and reactive oxygen species (ROS) levels. Additionally, it increased glutathione (GSH) levels and decreased protein carbonyl levels at the 900 mg/kg dose. The expression of interleukin-6 (IL-6) decreased at 900 mg/kg, tumor necrosis factor-alpha (TNF-α) levels dropped at 600 and 900 mg/kg, and the pro-apoptotic factor Bax was reduced at all doses. Sperm analysis showed improved sperm count and motility at the 900 mg/kg dose. Histological examination revealed significant positive effects of Citrulline on testicular tissue. Citrulline effectively lowers oxidative stress, inflammation, while enhancing sperm quality and pathological outcomes. These results indicate that Citrulline has potential as a therapeutic agent for testicular torsion.

Andrographolide prevents acute hyperammonemia-induced motor dysfunction in rats. Evidences for its mechanism of action

BackgroundBeside the cirrhotic one, non-cirrhotic hyperammonemia (HA) can also cause neuro-degeneration and establishment of 'Hyperammonemic Encephalopathy', ultimately leading to the coma stage. We have done pilot study on aqueous extract of Andrographis paniculata herb against HA induced oxidative stress in rats. Andrographolide (AGP) is the major component isolated from of A paniculata and reported to have various biological activities. PurposePresent study aimed to explore the therapeutic potentiality of AGP on rat model of non cirrhotic acute HA. MethodsRotarod and traction test was performed to access the motor function. Brain and serum ammonia level were assayed to confirm occurrence of HA. Malondialdehyde (MDA), reduced glutathione (GSH), protein carbonylation levels and activity of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR) were studied as oxidative stress markers. Expression of two NMDAR subunits, NR2A, 2B, nNOS and level of nitrite (NO2), cGMP in cerebral cortex and cerebellum were assayed to study the NMDAR-nNOS-cGMP cascade. ResultAcute HA caused motor dysfunction in rats. MDA level and protein carbonylation, increased significantly while SOD, catalase, GPx and GR got suppressed and NMDAR-nNOS-cGMP cascade activated in cerebral cortex and cerebellum. All these suggested establishment of hyperammonemic encephalopathy. AGP treatment restored the motor function, lowered the ammonia level, suppressed the oxidative stress markers, NR2A, 2B, nNOS over-expression and elevated NO2, cGMP levels in cortex and cerebellum. ConclusionOur study showed AGP could be a potential natural anti-hyperammonemic drug as it has prevented the development of acute hyperammonemic encaphalopathy in rats by suppressing NMDAR-nNOS-cGMP cascade and oxidative stress in cerebral cortex and cerebellum.

Source appointment and health risk assessment for atmospheric carbonyls in hot tropical city, Vietnam.

The aim of this study is to assess the spatiotemporal variation, sources, and health impacts of the carbonyl compounds (carbonyls) in Ho Chi Minh City (HCMC), the third-most populous city in Southeast Asia. Sampling was conducted according to the US.EPA Method TO-11A, from 2012 to 2016 in both the dry and the rainy seasons at twelve sites. The result shows that the carbonyl mixing ratios are high when compared to typical cities. Formaldehyde, acetaldehyde, and acetone are the most abundant carbonyls together accounting for 89% of the measured carbonyls. The carbonyl mixing ratio in rainy (46.0 ± 32.2ppb) is about twofold higher than that in dry (23.7 ± 10.3ppb). An inverse distance weighting method was adopted to map the spatial distribution of carbonyls across the city. The result shows that the carbonyl levels tended to be high in the city center. Three carbonyl sources are resolved by the PCA/APCS method: industrial sources and solvent usage (54%), vehicle exhausts (24%), cooking emissions (11%). Both lifetime cancer risk (LCR) and non-cancer hazard index (HIs) were calculated to estimate the health impacts on the community due to inhalation exposure to current carbonyl levels. The LCR values vary from 5.31 × 10-6 to 5.75 × 10-5 for formaldehyde higher than those of 6.61 × 10-7 to 1.36 × 10-5 for acetaldehyde, which mostly exceeded the US.EPA recommendation for five age groups. The hazard quotient values are 12.0 to 68.4 for acrolein, 0.44 to 2.84 for acetaldehyde, 0.55 to 1.85 for formaldehyde, and 0.13 to 0.89 for propionaldehyde.

From antioxidant to muscle enhancer: Resveratrol's role in grass carp (Ctenopharyngodon idella) nutrition

Resveratrol (RES), a type of stilbenoid, is known for its significant role in enhancing meat quality by virtue of activating SIRT1. Against this backdrop, this study explored the impact of resveratrol on various parameters influencing flesh quality in adult grass carp. Over a span of 9 weeks, adult grass carp were fed diets with five different levels of RES (0, 40, 80, 160 and 320 mg/kg). Our findings demonstrated that resveratrol supplementation had no adverse effects on the growth performance of adult grass carp. Notably, adding the right amount of resveratrol to the diets caused the protein and amino acid levels, pH24 h, and shear force of grass carp muscle to rise. Additionally, it led to a reduction in cooking loss and lactic acid content. Moreover, Addition of appropriate levels of resveratrol to the feed promoted myofiber hyperplasia in adult grass carp, which may be achieved by stimulating adult myoblast proliferation and differentiation. Subsequent studies have found that appropriate levels of resveratrol inhibit endoplasmic reticulum stress (ERS), which promotes muscle fiber development. Additionally, resveratrol was found to lead to an increase in unsaturated fatty acid (UFA) content in grass carp muscle. This alteration in fatty acid composition could be attributed to changes in fatty acid transport, synthesis, and catabolism. According to muscle protein carbonyl level, muscle protein content and frequency of muscle fibers smaller than 20 μm, the optimum resveratrol supplementations of grass carp were 178.33, 198.33 and 226.67 mg/kg.

Synergistic effect of curcumin and Piperine loaded Niosomal nanoparticles on acute pulmonary toxicity induced by Paraquat in mice.

Paraquat (PQ), a widely used non-selective herbicide, induces severe lung toxicity by promoting cell death and tissue necrosis through the generation of reactive oxygen species (ROS) and free radicals. This study aimed to develop and evaluate novel niosomal nanoparticles (NPs) encapsulating curcumin and piperine to mitigate PQ-induced acute pulmonary toxicity in Balb/c mice. The NPs were prepared using non-ionic surfactants and cholesterol via the thin film hydration method. Characterization revealed high encapsulation efficiency (>85%), proper particle sizes (264-286nm), narrow polydispersity index (PDI) (0.19±0.04 to 0.23±0.02), and good stability over 90days. Thermal analysis confirmed successful encapsulation of curcumin and piperine within the niosomal NPs. In vivo studies showed that PQ exposure significantly elevated ROS, lipid peroxidation (LPO), and protein carbonylation (PC) levels, while reducing glutathione (GSH) levels and impairing mitochondrial function (P<0.001). However, co-treatment with curcumin- and piperine-loaded niosomal NPs effectively reversed these effects (P<0.001), improving mitochondrial function. The combined formulation of curcumin and piperine in niosomal NPs offers a promising therapeutic strategy for treating PQ-induced pulmonary toxicity, likely due to enhanced bioavailability and potent antioxidant activity.