GPx Activity Research Articles

Exposure to the plasticizer diisopentyl phthalate can cause Vero cell line death

Phthalates are synthetic plasticizers present in the daily lives of humans, as part of the composition of different products, such as food packaging, water bottles, and toys. These compounds can migrate from plastic materials to the environment changing biological systems. Although diisopentyl phthalate (DiPeP) is largely used in Brazil, there is a lack of information on the possible toxic effects of this compound. This research aims to evaluate the toxicity of DiPeP in the Vero renal cells. These cells were exposed to the 1–1000 μM of DiPeP for 24 and 72 h and subsequently, the cytotoxicity, apoptosis and necrosis-inducing potential, and antioxidant system (SOD, GPx, and GST) were investigated. DiPeP neither caused cytotoxicity nor altered SOD and GPx activity, although GST has been increased at 100 or 1 μM (24 and 72 h, respectively). However, cell death by apoptosis and necrosis was observed. These results indicate that DiPeP caused cell death by a non-oxidative stress-mediated mechanism, which shows the relevance of investigate other process in further researches.

The RSM‐CCD Optimization of Fenton Process for Industrial Wastewater Treatment and Determination of Treatment Efficiency Using Some Biochemical Responses in Dreissena polymorpha

AbstractThe study investigated antioxidant biomarkers in Dreissena polymorpha to evaluate the efficiency of Fenton process (FP) in Organized Industrial Zone Wastewater (OIZW) treatment. Antioxidant enzymatic activities, including superoxide dismutase (SOD) and catalase (CAT), glutathione peroxidase (GPX), non‐enzymatic antioxidants (GSH) and the indicator of lipid peroxidation (TBARS) were measured in D. polymorpha in response to treated OIZW by FP. The performance of the FP has been optimized with response surface methodology (RSM). The optimum conditions (reaction time, and H2O2 and Fe2+ concentration) for OIZW by the FP process were determined. The results showed that the highest COD removal efficiency (83.94 %) was obtained when as Fe2+ concentration=402.35 mg/L, H2O2 concentration=4100.30 mg/L, and reaction time=10.10 min (desirability=1.000). SOD and CAT enzyme was decreased in the 1/25 diluted OIZW group compared to control group. CAT and SOD enzyme activities were increased after treatment compared to control groups. No statistically significant changes were observed in GSH levels and GPx activities. TBARS levels were increased 1/25 diluted OIZW exposure groups compared to the control group. TBARS levels were decreased after treatment. The results revealed that antioxidant parameters are useful biomarkers for determining the treatment efficiency of the FP.

Silver nanoparticles induce iron accumulation-associated cognitive impairment via modulating neuronal ferroptosis

Silver nanoparticles (AgNPs) are widely used in daily life and medical fields owing to their unique physicochemical properties. Daily exposure to AgNPs has become a great concern regarding their potential toxicity to human beings, especially to the central nervous system. Ferroptosis, a newly recognized programmed cell death, was recently reported to be associated with the neurodegenerative process. However, whether and how ferroptosis contributes to AgNPs-induced neurotoxicity remain unclear. In this study, we investigated the role of ferroptosis in neurotoxic effects induced by AgNPs using in vitro and in vivo models. Our results showed that AgNPs induced a notable dose-dependent cytotoxic effect on HT-22 cells and cognitive impairment in mice as indicated by a decline in learning and memory and brain tissue injuries. These findings were accompanied by iron overload caused by the disruption of the iron transport system and activation of NCOA4-mediated autophagic degradation of ferritin. The excessive free iron subsequently induced GSH depletion, loss of GPX and SOD activities, differential expression of Nrf2 signaling pathway elements, down-regulation of GPX4 protein and production of lipid peroxides, initiating ferroptosis cascades. The mitigating effects of ferrostatin-1 and deferoxamine on iron overload, redox imbalance, neuronal cell death, impairment of mice learning and memory, Aβ deposition and synaptic plasticity reduction suggested ferroptosis as a potential molecular mechanism in AgNPs-induced neurotoxicity. Taken together, these results demonstrated that AgNPs induced neuronal cell death and cognitive impairment with Aβ deposition and reduction of synaptic plasticity, which were mediated by ferroptosis caused by iron-mediated lipid peroxidation. Our study provides new insights into the underlying mechanisms of AgNPs-induced neurotoxicity and predicts potential preventive strategies.

Nanoselenium inhibits chromium toxicity in wheat plants by modifying the antioxidant defense system, ascorbate glutathione cycle, and glyoxalase system

Chromium (Cr) stress negatively impacts plant growth and physiological processes, making it a significant environmental concern. This study investigates the effectiveness of selenium nanoparticles (Se-NPs) in mitigating Cr stress on plants, comparing its efficacy with traditional selenium (Se). Nevertheless, research on using soil-applied Se-NP to lessen Cr buildup in plants has not been widely documented as of now. Here, we investigate the effectiveness of Se-NPs in mitigating Cr stress on plants, comparing their efficacy with traditional Se and control. Under the pervasive influence of Cr stress, Se-NPs exhibit remarkable superiority over conventional Se, significantly enhancing growth parameters (fresh weight, dry weight, shoot length, and root length), respectively, compared to the Cr-stressed plants. Physiologically, Se-NPs outperform Se by substantially improving the net photosynthesis rate (+32%), transpiration (+147%), and stomatal conductance (+64%), indicating its exceptional contribution to fortifying plant resilience under Cr stress. In mitigating oxidative stress, Se-NPs surpass Se, demonstrating a more pronounced reduction in LOX activity (−35%), MDA levels (−34%), H2O2 (−37%), and MG (−47%), showcasing heightened protection against Cr induced oxidative damage. Antioxidant defense systems also witness greater activation under Se-NPs, with higher increases in SOD (+27%), CAT (+54%), GPX (+7%), and GST (+37%) activities. Moreover, under Cr stress Se-NPs induce a more profound upregulation of antioxidant genes and the production of secondary metabolites, emphasizing its superior impact on the plant's defense mechanisms. The modulation of the ASA-GSH cycle by Se-NPs is more robust, with increased levels of ASA (+69%) and GSH (+33%), and decreased DHA (−28%) and GSSG (−29%), suggesting a more effective antioxidant network. Moreover, Se-NPs demonstrate heightened interference in Cr uptake in both root (−30%) and shoot tissues (−23%), indicating its potential to disrupt the Cr-induced ASA-GSH cycle. The study highlights the potential of Se-NPs as a more effective and sustainable approach to mitigate Cr-induced stress in plants, emphasizing the importance of understanding the underlying mechanisms and optimizing application strategies for improved agricultural sustainability and productivity in Cr-contaminated environments. Furthermore, it is necessary to conduct economic feasibility studies and assessments of the effects of Se-NP on soil microbiota in order to promote the widespread application in agricultural activities.

The germination response of Zea mays L. to osmotic potentials across optimal temperatures via halo-thermal time model

The maize (Zea mays L.) is a monocot that is a member of the Poaceae family and a valuable feed for livestock, human food, and raw material for various industries. The halothermal time model determines how plants respond to salt (NaCl) stress under sub-optimal conditions. This model examines the relation between NaClb (g), GR, GP, salinity and temperature stress on germination of seeds dynamics in various crops. Five constant temperatures i.e. 20, 25, 30, 35, and 40 °C and five ψ levels (NaCl concentrations converted to ψ − 0, − 0.2, − 0.4, − 0.6, and − 0.8 MPa) were used in this experiment. In light of the results, the maximum halo-thermal time constant value was recorded at 35 °C temperature, while maximum germination percentage was detected at 30 °C in the controlled condition. Moreover, the lowermost value was recorded at 20 °C at − 0.8 MPa osmotic potential. The highest CAT, APX, and GPX activities were recorded at 15 °C at − 0.8 MPa, while the lowest values were observed for 0 MPa at 30 °C temperature. In conclusion, by employing the halo thermal time model, the germination of maize variety (var.30W52) was accurately predicted for the first time under varying levels of temperature and osmotic potentials.

Umbilical cord blood thyroid hormones are inversely related to telomere length and mitochondrial DNA copy number

Hypothyroidism has been linked to reduced mortality rate and increased lifespan and health span. Telomere shortening, enhanced oxidative stress, and reduced cellular mitochondrial content are important hallmarks of aging shown to be related to age-associated diseases. It was proposed that the status of these markers in early life can be predictive of lifespan and the predisposition to certain age-associated disease in adulthood. Animal studies indicated that prenatal injection of thyroid hormones affects postnatal telomere length. Here, we sought to determine whether thyroid hormones TSH and fT4 are related to the telomere length, mitochondrial DNA copy number (mtDNAcn), and oxidative stress resistance marker GPX in the cord blood of newborns. In this study, we analyzed 70 mothers (18–42 years) and neonate dyads born in 2022 at the Nik Nafs maternity Hospital in Rafsanjan. The relative telomere length (RTL) and mtDNAcn were measured in the genomic DNA of cord blood leukocytes using real-time PCR. GPX enzyme activity was measured in the serum using colorimetric assays. In this study the correlation between these markers and the cord blood TSH and fT4 hormones were assessed using regression models. We found a reverse relationship between TSH levels and RTL in the cord blood of neonates. Additionally, our results displayed increased TSH levels associated with enhanced GPX activity. Regarding the mitochondrial DNA copy number, we found an indirect relationship between fT4 level and mtDNAcn only in male newborns. Future analyses of various oxidative stress markers, mitochondrial biogenesis status, telomerase activity, and the level of DNA damage are warranted to demonstrate the underlying mechanism of our observations.

Effect of trehalose treatment on growth, hydrogen peroxide, and antioxidant enzymes of Tomato (Solanum lycopersicum L.) plants under drought stress

The study was to determine the effect of trehalose treatment on growth, hydrogen peroxide and antioxidant enzymes in tomato plants growing under drought stress. In an experiment, the seeds were transferred to plastic pots, and the pots were divided into four groups. , the first and second groups without treatment 90%, 20% WHC (Water Holding Capacity)), while the third and fourth groups, 90%, 20% WHC In the presence of 25 mM trehalose (Tre). On day 30, plants were harvested, growth parameters, hydrogen peroxide (H2O2) and enzymes measured. Drought stress caused significant growth inhibition including fresh and dry weight, root length and shoot height. There was an increase in hydrogen peroxide and also an increase in the activity of some enzymatic antioxidants (SOD, CAT, and PPO) and a decrease of others (APx, GR, and GHPx) in the roots and stems of drought-stressed plants. Treatment with 25 mM trehalose significantly improved growth parameters compared to drought-stressed plants, and the results in this study showed a decrease in the activity of hydrogen peroxide (H2O2) and an increase in the activities of SOD, CAT, APx, GSHPx, GPx and PPO in the treated plants.

The Interplay of Dyslipidemia, Oxidative Stress, and Clinical Outcomes in Acute Ischemic Stroke Patients with and without Coronary Artery Disease.

We assessed lipid and lipoprotein profiles, along with oxidative stress (OS) parameters, in patients within the crucial 24 h period following an acute ischemic stroke (AIS), comparing those with and without coronary artery disease (CAD). We aimed to correlate these measures with clinical condition scales (NIHSS, mRS) post-AIS. This study included 27 AIS patients without CAD (AIS group) and 37 AIS patients with CAD (CAD-AIS group). Using polyacrylamide gel electrophoresis (Lipoprint system), we determined plasma LDL and HDL subfractions. Spectrophotometric methods were used to assess plasma antioxidant capacity, lipoperoxides, homocysteine (HC) levels, paraoxonase1, and catalase activities. We also measured urine isoprostanes and the activities of antioxidant enzymes (SOD, GPx) with commercial kits. CAD-AIS patients had notably higher HC levels, while there were no significant differences in lipoprotein subfractions and OS parameters between both groups. In the AIS group, mRS scores showed negative correlations with catalase, GPx activities, and total cholesterol. In the CAD-AIS group, atherogenic lipoproteins (IDLC, LDL2, LDL3-7) exhibited a significant positive correlation with mRS. This study underscores the role of dyslipidemia and OS in the development of AIS and CAD. It emphasizes the complex connections between specific biomarkers and post-stroke clinical outcomes. Our results suggest a significant impact of CAD treatment on lipid profile but not on homocysteine levels. The traditional narrative associating high cholesterol as the ultimate risk factor for cardiovascular diseases needs to be challenged, at least with respect to neurological outcomes. These insights may guide more targeted therapeutic approaches.

Tannic acid extracted from gallnut improves intestinal health with regulation of redox homeostasis and gut microbiota of weaned piglets

AbstractThe objective of this study is to evaluate the effects of tannic acid (TA) derived from gallnut supplementation on growth performance and health status of weaned piglets. A total of 432 weanling piglets (7.05 ± 1.05 kg) were randomly allocated into 4 treatment groups with 6 replicates of 18 pigs/pen. Piglets were fed either a basal diet (CON), or basal diets supplemented with 1.5 kg/t TA, 3.0 kg/t TA, or 1.8 kg/t zinc oxide (ZnO) for 21 days. The results showed that, compared to the CON, dietary TA supplementation did not affect (p > 0.05) growth performance and serum biochemistry of weaned piglets. However, 3.0 kg/t TA had higher SOD, GPX, and CAT activities and a lower MDA concentration in the jejunum than those of the CON or the ZnO group. Meanwhile, 3.0 kg/t TA increased (p < 0.05) villus height and villus height/crypt depth, and decreased (p < 0.05) crypt depth in the small intestine. Dietary TA also downregulated (p < 0.05) IL‐1β and TNF‐α expression in jejunum. Furthermore, 3.0 kg/t TA reduced (p < 0.05) the abundance of Candidatus Brocadia and Escherichia‐Shigella in cecal digesta. Notably, both Candidatus Brocadia and Escherichia‐Shigella had a negative correlation with antioxidant enzymes activities (R < −0.60, p < 0.01), but Escherichia‐Shigella was positively correlated with MDA concentrations (R = 0.44, p < 0.05) in the jejunum. In conclusion, compared to the CON, 3.0 kg/t TA supplementation improved the gut health status of weaned piglets, potentially by regulating redox homeostasis and gut microbiota.

The effects of short-time air pollution, SO2, and ozone on biochemical, histo-pathological, oxidative stress, and carcinogenesis related genes expressions in the liver of the rats.

Air pollution is a universal issue and has significant deleterious effects on both human health and also environment. The important indicators of air pollution include ozone (O3), particulate matter (PM), nitrogen dioxide (NO2), and sulfur dioxide (SO2). This research aims to investigate the impacts of ambient air pollution (AAP), SO2, and O3 on oxidative stress parameters, liver tissue histopathology, and expression of some carcinogenesis-related genes in the hepatic tissue of rats. 32 Wistar rats were randomly allocated to four groups: the control group, the AAP group, the SO2 group (10 ppm), and the ozone group (0.6 ppm). Over a period of five consecutive weeks, the rats were exposed to the specified pollutants for 3 h daily; liver tissues were harvested and instantly fixed with formalin. Pathological changes were assessed in the tissue samples. Additionally, the RT-qPCR technique was utilized to investigate Expression alterations of BAX, p-53, BCL2, caspase-3, caspase-8 and caspase-9. Furthermore, 30 milligrams of hepatic tissues were extracted to assess the activities of oxidative stress enzymes. The liver catalase and MDA activity were elevated in the air pollution (p < .05). Also, liver GPx activity in air pollution and ozone groups was significant in comparison to the control group (p < .05). The SO2 group exhibited severe lesions in histopathology examinations. The findings revealed an alteration in liver histopathology, an induction of oxidative stress, and the expression of some apoptosis-related genes in hepatic tissues after exposure to AAP, SO2, and O3.

Comparative toxic effect of ammonia exposure on Mauremys sinensis and invasive species Trachemys scripta elegans

As one of main pollutants, ammonia could cause adverse effects to aquatic animals. To explore the toxic effects of ammonia on Chinese striped-necked turtles (Mauremys sinensis) and invasive species red-eared slider (Trachemys scripta elegans), we compared the activities of antioxidant enzymes, the mRNA levels of genes involved in immune status, endoplasmic reticulum stress and apoptosis between T. s. elegans and M. sinensis under ammonia exposure for 30 days. The results showed that ammonia obviously increased the activities of SOD, CAT, GPX and T-AOC in both T. s. elegans and M. sinensis, especially CAT and GPX in T. s. elegans were higher than that in M. sinensis. The expression levels of JAK, RELA and Mcl-1 in T. s. elegans obviously increased, while IL-6 mRNA levels significantly increased in M. sinensis. In addition, Bip and IRE1 levels in M. sinensis showed a marked increase, and were significantly higher than that in T. s. elegans. Bcl-2 and Bcl-xL transcriptional levels in T. s. elegans showed an increase, especially Bcl-xL were significantly higher than that in M. sinensis. These results indicated that T. s. elegans exhibited more stronger antioxidant defense and immune function than M. sinensis under ammonia exposure. M. sinensis was more likely to occur endoplasmic reticulum stress and inflammation in ammonia environment. This research reveals the physiological response of turtles to ammonia, helps to understand adverse effects of environmental pressure on aquatic turtles, and further explains the tolerance of invasive species T. s. elegans to environmental pollution.

PM2.5 induce neurotoxicity via iron overload and redox imbalance mediated-ferroptosis in HT22 cells

PM2.5 is an important risk factor for the development and progression of cognitive impairment-related diseases. Ferroptosis, a new form of cell death driven by iron overload and lipid peroxidation, is proposed to have significant implications. To verify the possible role of ferroptosis in PM2.5-induced neurotoxicity, we investigated the cytotoxicity, intracellular iron content, iron metabolism-related genes, oxidative stress indices and indicators involving in Nrf2 and ferroptosis signaling pathways. Neurotoxicity biomarkers as well as the ferroptotic cell morphological changes were determined by Western Blot and TEM analysis. Our results revealed that PM2.5 induced cytotoxicity, lipid peroxidation, as indicated by MDA content, and neurotoxicity via Aβ deposition in a dose-related manner. Decreased cell viability and excessive iron accumulation in HT-22 cells can be partially blocked by ferroptosis inhibitors. Interestingly, GPX activity, Nrf2, and its regulated ferroptotic-related proteins (i.e. GPX4 and HO-1) were significantly up-regulated by PM2.5. Moreover, gene expression of DMT1, TfR1, IRP2 and FPN1 involved in iron homeostasis and NCOA4-dependent ferritinophagy were activated after PM2.5 exposure. The results demonstrated that PM2.5 triggered ferritinophagy-dependent ferroptotic cell death due to iron overload and redox imbalance. Activation of Nrf2 signaling pathways may confer a protective mechanism for PM2.5-induced oxidative stress and ferroptosis.

Antioxidant and antiproliferative effects of Teucrium polium extract: computational and in vivo study in rats

The current study aimed to assess the antioxidant and antiproliferative effects of teucrium polium extract: computational and in vivo study in rats. Three groups of animals: Group (i) constitute the control group; Group (ii) HeLa group received an intrafemoral inoculation of HeLa cells and Group (iii) constitue the combination between HeLa + T. polium. The plant was administered by gavage. Our results revealed that HeLa cell injection showed an elevation in aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin (TB), creatinine, urea, calcium and phosphorus. The pretreatment with the plant extract reduced the level of these parameters. Injection of HeLa cells showed a significant decrease in phosphorus and calcium respectively. However, the pretreatment by T. polium modulated the level of these two minerals. Rats treated with HeLa cells line showed an increase in the level of lipid peroxidation as evaluated by the TBARS substances, at the same time, a significant decreases in SOD, CAT and GPx activities were noted in the HeLa group compared to the control. On the other hand, pretreatment with the plant improved the level of these enzymes. Our results revealed that T.polium has a therapeutic effect on some health problems. HeLa cell line induced a small infiltration in liver and kidney. T. polium reduced the damage in both liver and kidney, but did not reveal any proliferation of tumor cells from trabecular bone tissue. The computational study revealed that T. polium compound bound with high free binding energies and established promising network of molecular interactions with COX-2 and TNF-α macromolecules.

Cleistocalyx nervosum var. paniala berry extract and cyanidin-3-glucoside inhibit hepatotoxicity and apoptosis.

Excessive oxidative toxicity in liver cells is a significant risk factor that can cause cellular injury, leading to the development of chronic liver disease (CLD). Natural anthocyanins have been shown to prevent the harmful effects of oxidative toxicity in mammalian cells. Ripe Cleistocalyx nervosum var. paniala berry fruits are rich in anthocyanins, which have been reported to possess many health benefits. Therefore, this study examined the protective effect of ethanolic fruit extract of C. nervosum var. paniala (CNPE) against hydrogen peroxide (H2O2)-induced oxidative damage and cell death in human hepatoma HepG2 cells. Results showed that CNPE had strong antioxidant capabilities and high amounts of total phenolics and anthocyanins. HPLC analysis showed that CNPE consists of cyanidin-3-glucoside (C3G). Our investigations found that HepG2 cells pretreated with CNPE or anthocyanin C3G inhibited H2O2-induced cellular damage and apoptosis by increasing the viability of cells, the expression of antiapoptotic Bcl-2 protein, and the activities of cellular antioxidant enzymes, namely SOD, CAT, and GPx. Moreover, both CNPE and C3G significantly suppressed expression of apoptotic proteins (Bax and cytochrome c) and the activities of cleaved caspase-9 and caspase-3 caused by H2O2. Our results indicate that CNPE and C3G can suppress H2O2-induced hepatotoxicity and cell death through stimulation of endogenous antioxidant enzyme activities and inhibition of apoptosis pathway in HepG2 cells. These findings might support development of CNPE as an alternative natural product for preventing CLD.

Biochemical and molecular assessment of oxidative stress in fruit fly exposed to azo dye Brilliant Black PN.

Azo dyes are widely used in the food industry to prevent color loss during processing and storage of products. This study aimed to investigate the effect of a diazo dye Brilliant Black PN (E151) on oxidative stress-related parameters in fruit flies (Drosophila melanogaster) at biochemical and molecular levels. Third instar larvae were transferred to a medium containing the dye at different doses (1, 2.5, and 5mg/mL). Gene expression and activity of superoxide dismutase, catalase (CAT), glutathione peroxidase (GPX), and acetylcholinesterase (AChE) enzymes were determined in the heads of adult flies obtained from these larvae. In addition, the glutathione (GSH) and malondialdehyde levels were measured using spectrophotometric analysis. Mitochondrial DNA (mtDNA) copy number was also detected by real-time PCR. The results showed that treatment with 5mg/mL of the dye caused a decrease in both gene expression and enzyme activity of CAT and GPx. Moreover, the same dose of dye treatment decreased AChE activity, GSH level, and mtDNA copy number. As a result, Brilliant Black PN dye can trigger toxicity by altering the level and activity of oxidative stress-related biomarkers in a dose-dependent manner. Therefore, more comprehensive studies are needed to elucidate the side effect mechanism and toxicity of this dye.

AKAP1 in Renal Patients with AHF to Reduce Ferroptosis of Cardiomyocyte.

This study mainly investigated the mechanism and effects of AKAP1 in renal patients with acute heart failure (AHF). Patients with renal patients with AHF and normal volunteers were collected. The left anterior descending arteries (LAD) of mice were ligated to induce myocardial infarction. AKAP1 messenger RNA (mRNA) expression was found to be down-regulated in renal patients with AHF. The serum levels of AKAP1 mRNA expression were negatively correlated with collagen I/III in patients. AKAP1 mRNA and protein expression in the heart tissue of mice with AHF were also found to be down-regulated in a time-dependent manner. Short hairpin (Sh)-AKAP1 promotes AHF in a mouse model. AKAP1 up-regulation reduces reactive oxygen species (ROS)-induced oxidative stress in an In Vitro model. AKAP1 up-regulation also reduces ROS-induced lipid peroxidation ferroptosis in an In Vitro model. AKAP1 induces NDUFS1 expression to increase GPX4 activity levels. AKAP1 protein interlinked with the NDUFS1 protein. Up-regulation of the AKAP1 gene reduced NDUFS1 ubiquitination, while down-regulation of the AKAP1 gene increased NDUFS1 ubiquitination in a model. In vivo imaging showed that the sh-AKAP1 virus reduced NDUFS1 expression in the heart of a mouse model. AKAP1 reduced ROS-induced lipid peroxidation ferroptosis through the inhibition of ubiquitination of NDUFS by mitochondrial damage in model of renal patients with AHF, suggest a novel target for AHF treatment.

The regulatory effects of pomiferin dietary on nickel-induced hepatic injury in Sprague–Dawley rats; action mechanisms and signaling pathways

The new technological applications of nickel (Ni) raise concerns over its harmful effects on the environment and human health. Pomiferin isolated from Osage orange is evaluated in in vitro and in vivo laboratory bioassays. This study focused the effects of pomiferin on Ni-caused hepatic injury and its underlying mechanisms. With this aim, Sprague–Dawley rats received 10 mg/kg nickel chloride (NiCl2) for 7 d by intraperitoneal injections. Pomiferin was given orally once a day at different doses (75, 150, and 300 mg/kg) for 20 d after exposure to NiCl2. Animals were anesthetized and livers were carefully collected to evaluate oxidative stress, inflammation, vascular injury, and hepatic function. Also, immunofluorescence analysis of apoptosis and DNA damage was performed on rat hepatic tissues. NiCl2 increased MDA production while reducing SOD, CAT, and GPx activity. NiCl2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. Moreover, there were significant increases in AST, ALT, and LDH levels. NiCl2 also caused significant pathological changes in hepatic. Additionally, it remarkably induced up-regulations of apoptotic marker and 8-OHdG expressions by immunofluorescence labeling in liver cells. Whereas, pomiferin significantly attenuated lipid peroxidation and increased antioxidant defense system in liver. Also, the use of pomiferin prevented deregulated inflammatory process by signaling pathways nuclear factor kappa B (NFκB)/COX-2/TNF-α/IL-1β/IL-6. In addition, pomiferin diminished histopathologic evidence of hepatic toxicity and significantly lower expressions of caspase 3 and 8-OHdG were observed in liver cells. Pomiferin seems to counteract the deleterious effects of NiCl2 on hepatic tissue through different cellular and signaling mechanisms.

Insulin improves spermatogenesis in a mouse model of aging

Aging can have adverse effects on the chance of fertility in men. In fact, men over 40 years old usually suffer from low sperm quality, sperm motility, and low level of serum testosterone that leads to infertility. In addition, the structure of DNA is more vulnerable in aged testes due to the high level of reactive oxygen species (ROS) and nitric oxide. However, it has been showed that insulin is able to decrease oxidative stress and apoptosis. Moreover, some studies showed that insulin can enhance both spermatogenesis and fertility. In this regard, we investigate the impacts of insulin on spermatogenesis, the number of sperm, and the level of gonadal hormones in aged testes of mice. Thirty-six adult male NMRI mice were used. They were kept under standard conditions. The animals were divided into two groups control and insulin. The insulin group received 100 µL insulin with a 72-hour interval by intraperitoneal (IP) injection for 33 weeks and the control group received water. At the 8, 12, and 33 weeks of treatment, the testes of mice were removed for histological, cellular (ROS and glutathione [GSH]) and molecular (Bcal2, caspase-3, and Bax) analysis. For measurement of the level of hormones (testosterone, LH, and FSH), the blood samples were collected from the heart. According to our findings, insulin could significantly increase the volume of the testes and the total number of spermatogonial stem cells, primary spermatocytes, round spermatids as well as leydig cells. In addition, activity of GPX was considerably high in the insulin group. Furthermore, in the insulin group, the level of ROS was reduced. In conclusion, insulin may be effective in enhancing the function of the testes in aged male mice.

Assessing the impact of dietary polystyrene nanoplastics on growth performance, immunological parameters, and antioxidant defense in zebrafish (Danio rerio)

AbstractThis trial was performed in order to investigate the response of zebrafish (Danio rerio) to dietary exposure to polystyrene nanoplastics (PS‐NPs) under laboratory conditions on fish growth and health. Healthy zebrafish (n=240) were divided into 12 tanks and fed with diets including 0 (T0), 100 (T1), 500 (T2), and 1000 (T3) mg kg−1 synthesized polystyrenes nanoplastics (PS‐NPs) for 30 days. At the end of trial, fish fed the PS‐NPs supplementation showed weight gain percentages of 79.45%, 70.35%, and 61.88% for T1, T2, and T3 groups, respectively, compared with 87.39% in the control fish. The SOD, GPX and MDA activities and cortisol levels increased by 47%, 32% and 35% and 46%, respectively, especially at high‐dose administration (p &lt; 0.05). The expression of GPX (T2‐81% and T3‐82%) and SOD (T2‐101% and T3‐187%) were remarkably upregulated in T2 and T3 groups. Moreover, the relative gene expression of HSP70, interleukin‐1 (IL1), Interferon γ (IFN‐γ) and tumor necrosis factor‐α (TNF‐α) increased by 178%, 202%, 154% and 307%, respectively, especially at high‐dose administration (p &lt; 0.05). The results of the present study demonstrated that exposure to PS‐NPs especially at high concentrations (500 and 1000 mg kg−1 of diet) negatively influenced growth, health status‐, antioxidant‐, and immunity‐related gene expression responses of zebrafish.

Effects of Exposure to Urban Atmospheric Particulate Matter Suspended in Seawater on the Mussel Mytilus galloprovincialis

Atmospheric particulate matter (PM) contains numerous constituents, including organic molecules, inorganic ions, and metals, with some of them possessing hazardous properties. Although mainly associated with air pollution, PM can rapidly be transferred from air and land to aquatic ecosystems, and consequently poses a risk to marine biota. The aim of this work was to evaluate how urban atmospheric PM (a standard reference mixture of urban PM, known to contain various organic and inorganic contaminants), suspended in seawater, may cause toxicity in marine organisms. To this purpose, mussels (Mytilus galloprovincialis) were exposed to two concentrations of suspended PM: 5.7 and 11.4 mg/L. After 7, 14, and 21 days, the animals were collected and the gills and digestive gland were analysed for stress biomarkers (CAT, SOD, GPX, GST, MDA, and Ubi). In general, the results show that exposure to different concentrations of PM caused an increase in GST, UBI, and GPx activities compared to their respective controls. The average activities of GST (87.65 ± 30.23 nmol/min/mg of total protein) in the gills of the animals exposed to 11.4 mg/L of PM increased after 21 days of exposure, and the activity of GPx (8.04 ± 3.09 nmol/min/mg of total protein) in the gills increased after 14 days in the animals exposed to 5.7 mg/L of PM. MDA results also provided information on cellular damage, with the most pronounced effects being found in the gills of exposed mussels. This study confirms that mussels are useful as “early warning” indicators of environmental contamination and provides important information on the effects of PM on marine biota.