Depletion Of Antioxidants Research Articles

Ferulic acid protects HepG2 cells and mouse liver from iron-induced damage

Liver as iron storage organ is particularly susceptible to oxidative stress-induced injury from excess iron. Thus, antioxidant therapies are often used to reverse oxidative damage and protect cells and tissues. This study investigated the protective effects of phenolic acids; ferulic acid (FA) and its metabolite, ferulic acid 4-O-sulfate disodium salt (FAS) against oxidative stress under iron overload conditions in mouse and HepG2 cells. Cells were exposed to FA or FAS and then treated with iron-induced oxidative stress complex of 50 μmol/L FAC and 20 μmol/L of 8-hydroxyquinoline 8HQ (8HQ-FAC). Iron dextran was injected intraperitoneally on alternate days for 10 days to induce the iron overload condition in BALB/c mice. The study revealed that the phenolic acids were protective against ROS production, lipid peroxidation and antioxidant depletion in HepG2 cells and liver tissues of BALB/c mice during iron-induced oxidative stress. The protective function of phenolic acids was achieved by the transcriptional activation of nuclear factor erythroid-2-related factor 2 (Nrf2) to regulate antioxidant genes. In conclusion, the study provides evidence that FA has the potential as a therapeutic agent against iron-related diseases such as T2D.

Longevity of multilayered textured HDPE geomembranes in low-level waste applications

The degradation behaviour of five multilayered textured white geomembranes (GMBs) is investigated when immersed in two synthetic low-level waste (LLW) leachates with pH 7 and 9 at a range of temperatures (40–85 °C) for 48–55 months. Results are compared to the performance of the GMBs in synthetic municipal solid waste (MSW) leachate. Increasing pH from 7 to 9 gives slightly faster antioxidant depletion in LLW leachate. The estimated time to nominal failure for the GMBs is at least 20% longer in LLW leachate than in MSW leachate containing surfactant that accelerates both antioxidant depletion and stress cracking. Thus, MSW leachate can be used as a conservative proxy to estimate the service life of a GMB in contact with LLW leachate. Two GMBs are considered very highly likely to meet the required 550 year design life of the near-surface disposal facilities even based on the most conservative prediction of the time to nominal failure for the GMBs.

Concurrent administration of farnesol protects acetaminophen-induced acute hepatic necrosis in mice.

Acetaminophen (APAP) is known to cause acute liver injury and acute liver failure in Western countries. This study investigates the protective role of farnesol (FAR) (C15 H26 O), a natural sesquiterpene alcohol in essential oils, against APAP-induced acute liver necrosis in mice. Mice were injected with a single dose of APAP (300 mg/kg) via an intraperitoneal route. Different groups of mice were concurrently treated with a single dose of FAR 25 mg/kg, FAR 50 mg/kg, and N-acetylcysteine. APAP administration caused a significant increase in transaminase activities and malondialdehyde (MDA) levels in the serum and liver tissue, respectively, with a concomitant decrease inintracellular antioxidants, including reduced glutathione (GSH) in the liver tissue. APAP intoxication upregulated proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1β(IL-1β), IL-6, nuclear factor-κB (NF-κB), and IκB kinase β in the liver tissue. FAR and N-acetylcysteine (NAC) administrations concurrently with APAP preventedserum transaminase increase in serum and MDA levels in the liver tissue. A high dose of FAR and NAC treatments significantly inhibited GSH and other antioxidant depletion. FAR and NAC treatments also downregulated the expression of proinflammatory markers. FAR treatments protects against APAP-induced acute liver injury and offers antioxidant and anti-inflammatory effects by inhibiting the NF-κB pathway involved in the transcription of genes responsible for inflammatory cytokine synthesis.

Suppression of Helicobacter pylori-induced gastric carcinogenesis by emodin in GES-1 cells through the PI3K/AKT and NRF2 signaling pathways

Helicobacter pylori is recognized as a microbial carcinogen among Gram-negative bacteria and is considered the most significant risk factor for the development of human gastric cancer (GS). Consequently, inhibiting the growth of H. pylori has become a critical strategy for preventing GS. This study focuses on the inhibitory effects of emodin (EMN) against H. pylori-induced gastric carcinogenic signaling in human gastric epithelial cells (GES-1). In vitro cytotoxicity assessments revealed that a concentration of 40 μM of EMN provided remarkable protection to gastric cells, resulting in 85% cell viability without inducing toxicity. Furthermore, EMN prevented the H. pylori-induced depletion of antioxidants, which was mediated by reactive oxygen species generation, DNA damage, and nuclear fragmentation. Our findings indicate that EMN significantly suppresses the expression of phosphorylated forms of phosphatidylinositol 3-kinase (PI3K)/AKT, phosphorylated p38 kinases (p-p38), phosphorylated extracellular signal-regulated kinase-1 (p-ERK1), phosphorylated c-Jun N-terminal kinase (p-JNK) in GES-1 cells infected with H. pylori. In addition, EMN notably enhances the expression of antioxidant proteins nuclear factor erythroid factor-2 (NRF2) in H. pylori-infected cells. In summary, EMN demonstrates promising potential in preventing H. pylori-associated infections and the subsequent development of resistance, making it a viable candidate for the prevention of H. pylori-induced GS.

Frequency of application of 24-epibrassinolide on plant growth, physiology and postharvest fruit quality of Cantaloupe grown at elevated temperature

ABSTRACT Reduction of yield in tropical greenhouses is an issue with Cucumis melo L. var. cantaloupensis. A natural occurring hormone, 24-epibrassinolide (EBR), regulates cellular activities and physiological processes of plants and signaling. To determine effects of EBR application, cantaloupe cvs. Himalai-99 and Glamour (factor 1) were treated with 0.1 mg∙L−1 EBR applied over four frequencies (factor 2) as; F1: no EBR (control), F2: at 15 DAT (days after transplant), F3: at 15 + 30 DAT, and F4: at 15 + 30 + 45 DAT at 47 ± 3°C (5°C higher than the ambient greenhouse) in a factorial Randomized Complete Block Design (RCBD) with four replicates. Postharvest fruit quality was monitored at room temperature (26°C) in a completely randomized design with four replicates. Data were analyzed using Analysis of Variance, mean separation with least significant difference and associations between parameters with Pearson correlation. Application of EBR at 15 + 30 DAT (F3) increased plant dry weight, leaf area, specific leaf area, root length, root surface area, photosynthesis rate, stomatal conductance, transpiration rate and chlorophyll content. It increased the quantum efficiency of photosystem II, peroxidase and catalase activities by 50%, stomatal length and width by 75% and decreased malondialdehyde and proline content by 56%. Pre-harvest foliar application of EBR at 15 + 30 DAT reduced postharvest weight loss and ethylene emission rate by two fold and reduced ascorbic acid and antioxidant depletion rates during storage. The EBR application at 15 + 30 DAT produced the best plant and fruit quality performances, while the application of EBR at fruit development stage (45 DAT) caused reduced fruit quality.

Berberine mitigates acetamiprid-induced hepatotoxicity and inflammation via regulating endogenous antioxidants and NF-κB/TNF-α signaling in rats.

Acetamiprid is a neonicotinoid insecticide used on a large scale and has been reported for oxidative stress-mediated toxicity and physiological alterations in mammals. The plant-derived natural antioxidant berberine (BBR) possesses protective potential against inflammation, structural changes, and cellular toxicity. The current study aimed to investigate the toxic effects of acetamiprid exposure and the antioxidative and anti-inflammatory efficacy of BBR in rat liver tissue. The results showed that intragastric exposure of acetamiprid (21.7mg/kg b.wt, i.e., 1/10 of LD50) for 21days significantly elicited oxidative stress as evidenced by lipid peroxidation, protein oxidation, and depletion of endogenous antioxidants. Furthermore, acetamiprid exposure elevated NF-κB, TNF-α, IL-1β, IL-6, and IL-12 expression and caused structural alterations in liver tissue. Biochemical results showed that 2-h pre-treatment of BBR (150mg/kg b.wt; 21days) reduced damage to lipids and proteins, replenished GSH, enhanced SOD and catalase activities, and offered antioxidative effects against acetamiprid toxicity. Also, BBR suppressed inflammation by regulating NF-κB/TNF-α signaling in hepatic tissue of acetamiprid-intoxicated rats. Histopathological examination confirmed the hepatoprotective effects of BBR. Our findings indicate that BBR might be a potential ameliorative agent against oxidative stress-mediated hepatotoxicity.

Zinc and L-carnitine combination with or without methotrexate prevents intestinal toxicity during arthritis treatment via Nrf2/Sirt1/Foxo3 pathways: an In vivo and molecular docking approach.

Methotrexate (MTX) is an antifolate that is inescapable and widely used to treat autoimmune diseases and is the gold standard medicine for the arthritic condition. Despite its importance, it is more prone to gastrointestinal toxicity, which is most common in arthritis patients during MTX treatment. Combination therapies are required to ensure MTX's antiarthritic activity while providing gastrointestinal protection. Zinc (Zn) and L-carnitine (Lc) are well-known potent antioxidants and anti-inflammatory supplements with promising results in pre-clinical studies. Arthritis was induced in Wistar rat's ankles with Freund's adjuvant and treated with either MTX (2.5mg/kg b.w per week for two weeks) or Zn (18mg/kg b.w. per day) Lc (200mg/kg b.w. per day) individually or in combination (MTX + Zn Lc). The antiarthritic effects were evaluated by body weight, paw volume, ankle tissue, and joint histopathology. At the same time, anti-toxicity/gastrointestinal protective activity was examined by tissue oxidative stress markers, antioxidants, mitochondrial function, inflammatory mediators, and antioxidant signaling proteins and their binding mechanism. Repercussions of MTX intoxication induced upregulation of oxidative stress markers, antioxidant depletion, ATP depletion, decreased expression of Nrf2/Sirt1/Foxo3, and the overexpression of inflammatory mediators attenuated by co-treatment with Zn Lc. Zn Lc markedly mitigated MTX-instigated intestinal injury by activating antioxidant signaling mechanisms Nrf2/Sirt1/Foxo3 signaling and tissue architectural anomalies and exhibited an enhanced antiarthritic effect. In conclusion, we report that Zn Lc and MTX combination could presumably protect the intestine from low-dose MTX which managed arthritis but induced severe intestinal damage with increased inflammation and downregulated Nrf2/Sirt1/Foxo3 pathway.

Cerebral-Organoid-Derived Exosomes Alleviate Oxidative Stress and Promote LMX1A-Dependent Dopaminergic Differentiation.

The remarkable advancements related to cerebral organoids have provided unprecedented opportunities to model human brain development and diseases. However, despite their potential significance in neurodegenerative diseases such as Parkinson's disease (PD), the role of exosomes from cerebral organoids (OExo) has been largely unknown. In this study, we compared the effects of OExo to those of mesenchymal stem cell (MSC)-derived exosomes (CExo) and found that OExo shared similar neuroprotective effects to CExo. Our findings showed that OExo mitigated H2O2-induced oxidative stress and apoptosis in rat midbrain astrocytes by reducing excess ROS production, antioxidant depletion, lipid peroxidation, mitochondrial dysfunction, and the expression of pro-apoptotic genes. Notably, OExo demonstrated superiority over CExo in promoting the differentiation of human-induced pluripotent stem cells (iPSCs) into dopaminergic (DA) neurons. This was attributed to the higher abundance of neurotrophic factors, including neurotrophin-4 (NT-4) and glial-cell-derived neurotrophic factor (GDNF), in OExo, which facilitated the iPSCs' differentiation into DA neurons in an LIM homeobox transcription factor 1 alpha (LMX1A)-dependent manner. Our study provides novel insight into the biological properties of cerebral organoids and highlights the potential of OExo in the treatment of neurodegenerative diseases such as PD.

Environmentally relevant doses of endocrine disrupting chemicals affect male fertility by interfering with sertoli cell glucose metabolism in mice

The growing global deterioration in several aspects of human health has been partly attributed to hazardous effects of endocrine-disrupting chemicals (EDCs) exposure. Therefore, experts and government regulatory agencies have consistently advocated for studies on the combined effects of EDCs that model human exposure to multiple environmental chemicals in real life. Here, we investigated how low concentrations of bisphenol A (BPA), and phthalates compounds affect the Sertoli cell glucose uptake/lactate production in the testis and male fertility. An EDC mixture containing a detected amount of each chemical compound in humans, called daily exposure (DE), and DE increased in magnitude by 25 (DE25), 250 (DE250), and 2500 (DE2500), and corn oil (control) were administered for six weeks to male mice. We found that DE activated estrogen receptor beta (Erβ) and glucose-regulated protein 78 (Grp 78) and disrupted the estradiol (E2) balance. In addition, DE25, DE250, and DE2500 doses of the EDC mixture via binding with Sertoli cells’ estrogen receptors (ERs) inhibited the glucose uptake and lactate production processes by downregulating glucose transporters (GLUTs) and glycolytic enzymes. As a result, endoplasmic reticulum stress (ERS), marked by unfolded protein response (UPR) activation, was induced. The accompanying upregulation of activating transcription factor 4 (ATF4), inositol requiring enzyme-1 (IRE1), C/EBP homologous protein (CHOP), and mitogen-activated protein kinase (MAPK) signaling promoted antioxidant depletion, testicular cell apoptosis, abnormal regulation of the blood−testis barrier, and decreased sperm count. Therefore, these findings suggest that human and wildlife exposure to multiple environmental chemicals can produce a wide range of reproductive health complications in male mammals.

Effect of Ficus carica extract on hematological parameters and antioxidant defense system in erythrocytes of albino rats exposed to nickel chloride

Heavy metals including nickel have adverse effects on hematological system and red blood cells antioxidant defense. The purpose of the study is to examine the possible corrective effect of fig (Ficus carica L.) extract (FCE) on hematological parameters and antioxidant enzyme activities in red blood cells of rats exposed to sub-lethal concentration of nickel. Male Wistar rats were exposed to nickel chloride (10 mg/kg) and then treated or no with FCE (350 mg/kg) for 4-weeks. The intoxication induces alteration of haematological parameters and enhances blood haemolysis, generates oxidative stress induced decrease in the antioxidant enzyme activities and depletion in reduced glutathione levels in intoxicated group compared to the control group. The oral administration of FCE increase significantly hemoglobin levels (Hb), red blood cells count (RBC), hematocrit (Ht) and decreases white blood cells counts (WBC), and platelets in F. carica treated groups, and also the extract increase the GSH-Px and SOD antioxidant activity, GSH reserves in red blood cells, and reduces lipids peroxidation. The present study concludes that fig fruits may exhibit potent antioxidant potential for erythrocytes and have a positive effect on hematological system.

Adsorption of l-buthionine sulfoximine on Bi(III) and Eu(III) co-substituted hydroxyapatite nanocrystals for enhancing radiosensitization effects

Cancer theranostics combines therapeutic and diagnostic capabilities into a single system to treat cancer efficiently. Biocompatible nanomaterials can be engineered to exhibit cancer theranostic functions, for instance radiosensitization and photoluminescence. In this study, trivalent Bi and Eu ions were co-substituted into the lattice of hydroxyapatite (Bi(III):Eu(III) HAp) to develop a cancer theranostic nanocrystal. Bi provides radiosensitization capabilities while Eu imparts photoluminescence properties. To complement the radiotherapeutic function, l-buthionine sulfoximine (l-BSO) was adsorbed onto the nanocrystal surface. l-BSO inhibits the biosynthesis of cellular antioxidants, which can enhance radiosensitization effects. The Bi(III):Eu(III) HAp nanocrystals were prepared via a hydrothermal method. Structural and compositional analyses showed that both Bi and Eu ions were substituted into the HAp lattice. l-BSO was adsorbed onto the surface via electrostatic interactions between the charged carboxyl and amino groups of l-BSO and the surface ions of the nanocrystals. The adsorption followed the Langmuir isotherm model, implying a homogeneous monolayer adsorption. The l-BSO adsorbed Bi(III):Eu(III) HAp nanocrystals were found to have negligible cytotoxicity except the setting with l-BSO adsorbed amounts of 0.44 μmol/m2. This l-BSO amount was found to be high enough to elicit cytotoxicity due to l-BSO being released and causing excessive antioxidant depletion. Gamma ray irradiation clearly activated the cytotoxicity of the samples and increased the cell death rate, confirming radiosensitization abilities. At a constant amount of nanocrystals, the cell death rate increases with l-BSO concentration. This indicates that l-BSO can enhance the radiosensitization effect of the Bi(III):Eu(III) HAp nanocrystals.

Synergistic toxicity of NiO nanoparticles and benzo[a]pyrene co-exposure in liver cells: Role of free oxygen radicals induced oxidative stress

Current attention has been given on health effects of combined exposure of nanoscale materials and organic pollutants. Nickel (II) oxide nanoparticles (NiO NPs) displays exceptional properties and is being used in various areas such as batteries, diesel–fuel additives, and biomedicals. Benzo[a]pyrene (BaP) is a ubiquitous pollutant. Cigarette smoke, diesel exhaust, and grilled foods are main sources of BaP exposure. Therefore, combined exposure of NiO NPs and BaP to humans is unavoidable. There is a dearth of knowledge on combined effects of NiO NPs and BaP in humans. This study was aimed to investigate co-exposure effects of NiO NPs and BaP in human liver cells (HepG2) and primary rat hepatocytes. We observed that individual and co-exposure of NiO NPs and BaP induced cytotoxicity, lactate dehydrogenase leakage, lipid peroxidation, depletion of mitochondrial membrane potential, and activation of caspases (-3 and -9) in both types of cells. Individual and co-exposure of NiO NPs and BaP further accelerated the generation of free oxygen radicals (reactive oxygen species and hydrogen peroxide) and depletion of antioxidants (glutathione and various antioxidant enzymes). Remarkably, NiO NPs and BaP exerted synergistic toxicity to both HepG2 cells and primary rat hepatocytes. Moreover, combined toxicity of NiO NPs and BaP in both cells was mediated through free oxygen radicals induced oxidative stress. This work warrants further research on risk assessment of co-exposure effects NiO NPs and BaP in an appropriate in vivo model.

Tannic Acid Mitigates Rotenone-Induced Dopaminergic Neurodegeneration by Inhibiting Inflammation, Oxidative Stress, Apoptosis, and Glutamate Toxicity in Rats.

Parkinson's disease (PD), a movement disorder, is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) region of the brain. The etiopathogenesis of PD involves increased oxidative stress, augmented inflammation, impaired autophagy, accumulation of α-synuclein, and α-Glutamate neurotoxicity. The treatment of PD is limited and there is a lack of agents to prevent the disease/delay its progression and inhibit the onset of pathogenic events. Many agents of natural and synthetic origin have been investigated employing experimental models of PD, mimicking human PD. In the present study, we assessed the effect of tannic acid (TA) in a rodent model of PD induced by rotenone (ROT), a pesticide and an environmental toxin of natural origin reported to cause PD in agricultural workers and farmers. Rotenone (2.5 mg/kg/day, i.p.) was administered for 28 days, and TA (50 mg/kg, orally) was administered 30 min before ROT injections. The study results showed an increase in oxidative stress, as evidenced by the depletion of endogenous antioxidants and enhanced formation of lipid peroxidation products, along with the onset of inflammation following a rise in inflammatory mediators and proinflammatory cytokines. ROT injections have also augmented apoptosis, impaired autophagy, promoted synaptic loss, and perturbed α-Glutamate hyperpolarization in rats. ROT injections also induced the loss of dopaminergic neurons subsequent to the activation of microglia and astrocytes. However, TA treatment was observed to reduce lipid peroxidation, prevent loss of endogenous antioxidants, and inhibit the release and synthesis of proinflammatory cytokines, in addition to the favorable modulation of apoptosis and autophagic pathways. Treatment with TA also attenuated the activation of microglia and astrocytes along with preservation of dopaminergic neurons following reduced loss of dopaminergic neurodegeneration and inhibition of synaptic loss and α-Glutamate cytotoxicity. The effects of TA in ROT-induced PD were attributed to the antioxidant, anti-inflammatory, antiapoptotic, and neurogenesis properties. Based on the present study findings, it can be concluded that TA may be a promising novel therapeutic candidate for pharmaceutical as well as nutraceutical development owing to its neuroprotective properties in PD. Further regulatory toxicology and translational studies are suggested for future clinical usage in PD.

Assessing the chemical composition, potential toxicity and cancer risk of airborne fine particulate matter (PM2.5) near a petrochemical industrial area

In the vicinity of a petrochemical industrial region in São Paulo, Brazil, PM2.5-bound organic carbon (OC), elemental carbon (EC), polycyclic aromatic hydrocarbons (PAHs), nitro-PAHs, oxy-PAHs, hopanes, and inorganic species were evaluated. Oxidative potential (OP), burden (OB), and Alivibrio fischeri bioluminescence inhibition (AFBIA) assays were conducted to determine the potential health effects of exposure to these compounds. The PM2.5 mean concentration was 32.0 ± 18.2 µg m−3, and benzo (a)pyrene was found to exceed recommended levels by at least four times. Secondary sources and vehicular emissions were indicated by nitro-PAHs, oxy-PAHs, and inorganic species. The OP and OB results revealed that secondary compounds favored antioxidant depletion. The AFBIA results showed that 64 % of the samples were toxic. These findings emphasize the need to reduce the exposure risk and take measures to protect human health.

Combined ROS-related therapy improves the efficacy of multipleneoantigen vaccines against LUAD

Lung adenocarcinoma (LUAD) is classified as Non-Small-Cell Lung Cancer (NSCLC), one of the most malignantcancers due to its poor prognosis and fast progression. Its resistance to chemotherapy, immunosuppressive tumormicroenvironment (TME), and frequent immune evasion also impose enormous obstacles in treating LUAD. However,previous research found that these tumor cells resistant to chemotherapies commonly increase their production ofintracellular reactive oxygen species (ROS) due to high mitochondria activity. Antioxidants like glutathione (GSH)are also highly produced to maintain their redox homeostasis. Therefore, the depletion of antioxidants which can leadto intratumoral accumulation of ROS to cytotoxic levels, provides a new therapeutic target. Besides, the high levelof extracellular ROS also significantly contributes to the immunosuppressive characteristic of TME, which exhaustsactivated T cells. This work provides the framework for a novel combinational therapy based on a multiple-neoantigenvaccine to avoid immune evasion. Two types of nanoparticles further boost the vaccine’s efficacy against tumors, onedepleting intratumoral GSH and scavenging extracellular ROS. Anticipated results are shown from various aspects,hoping the innovative treatment can effectively improve the survival rate with few side effects.

Enhancement of oxidative stress, oxidative dna damage and lowered pefr in gasoline station attendants in calabar metropolis

Exposure to gasoline fumes through inhalation or accidental ingestion has been associated with chronic inflammatory reactions leading to oxidative stress, oxidative DNA damage and increased risk of chronic lung conditions and cancer. This study assessed the peak expiratory flow rate (PEFR) and biomarkers of oxidative stress (total antioxidant capacity (TAC), total plasma peroxides (TPP), oxidative stress index (OSI)), oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)), 1-hydroxypyrene and urine creatinine in Gasoline Station Attendants. A total of 100 consenting adults, aged 18-60 years, comprising 50 gasoline station attendants and 50 non-gasoline station attendants (controls) were enrolled into this comparative cross-sectional study. The PEFR was determined using the peak flow meter, TAC, TPP and creatinine by colorimetry, 8-OHdG by enzyme linked immunosorbent assay (ELISA), 1-hydroxypyrene (1-HOP) by high performance liquid chromatography and OSI by calculation. Data was analysed using unpaired Student t-test and Pearson's correlation analysis at p<0.05.
 The body mass index, TPP, OSI and 8-OHdG levels were significantly higher and TAC and PEFR lower in gasoline pump attendants compared to the control groups (p<0.05). Positive correlations were observed between TPP and years at work (r=0.638, p=0.000), between TPP and OSI (r=0.282, p=0.047) and negative correlation between TAC and OSI (r=-0.555, p=0.000) only in gasoline station attendants. Exposure to gasoline is associated with increased lipid peroxidation and oxidative DNA damage, reduced lung function and depletion of antioxidants which may result in oxidative stress and increased risk for the development of chronic lung conditions in gasoline station attendants.

Is Cataract in Patients under 60 Years Associated with Oxidative Stress?

Oxidative stress is considered as a possible factor in the genesis of cataract. The study aimed to determine the systemic antioxidant status in cataract patients under 60 years. We studied 28 consecutive cataract patients, mean of 53 years (SD = 9.2), a range of 22-60 and 37 controls. In erythrocytes, activity of antioxidant enzymes was determined: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), in contrast with plasma concentrations of vitamin A and E. Conjugated dienes (CD) level and protein carbonyls (PC) concentration were also determined in plasma. Malondialdehyde (MDA) concentrations in erythrocytes and plasma were also measured. SOD and GPx activity and vitamin A and E concentrations were lower in cataract patients (p = 0.000511, 0.02, 0.022, and 0.000006, respectively). MDA plasma and erythrocytes concentrations were higher in cataract patients (p = 0.000001 and 0.0000001, respectively). PC concentration was higher in cataract patients than in controls (p = 0.00000013). There were statistically significant correlations between oxidative stress markers both in the cataract patients group as well as in the control group. Cataract incidence in patients under 60 years seems to be accompanied by enhanced lipid peroxidation and protein oxidation, as well as antioxidant defense depletion. Thus, supplementation with antioxidants could be beneficial in this group of patients.

The effect of dietary Crataegus Sinaica on the growth performance, immune responses, hemato-biochemical and oxidative stress indices, tissues architecture, and resistance to Aeromonas sobria infection of acrylamide-exposed Clarias gariepinus

This study investigated the effect of using a natural dietary supplement of Crataegus Sinaica (CS) to mitigate the negative impacts of waterborne acrylamide (ACR) on the health and performance of freshwater fish, African catfish (Clarias gariepinus). For this aim, 270 fish were divided into six groups (45 fish/group). Three groups were kept in non-contaminated water and fed a non-fortified basal diet, 1% CS, and 2% CS. The other three groups were exposed to ACR (26.6 mg/L water) and fed a basal diet, 1% CS, and 2% CS. After 60 days, the growth performance, liver and kidney function, stress indicators, oxidative stress indices, immunological response, vital tissue architecture, and resistance to Aeromonas sobria have been evaluated. Results indicated that CS dietary supplementation (1% and 2% CS) significantly counteracted ACR-induced reduced growth and survival. Furthermore, both CS dietary supplementation significantly balanced the ACR-induced leukopenia, anemia, hypoalbuminemia, hypoglobulinemia, and hypoproteinemia. Likewise, 1% and 2% CS addition to the ACR-exposed fish diets significantly reduced the ACR-induced increase in serum enzymes, bilirubin, renal damage products, hyperglycemia, and cortisol. Instead, the ACR-evoked depletion of antioxidant (glutathione peroxidase, superoxide dismutase, catalase, and reduced glutathione) and innate immune (lysozyme, complement3, and nitric oxide) components were significantly restored by both CS dietary supplementation. Besides, the ACR-induced pathological alterations in hepatic, renal, and splenic tissues were considerably lessened by CS. Besides, the reduced disease resistance of ACR-exposed fish was restored when challenged with A.sobria in a fish-fed 1% and 2% CS-fortified diet. Noteworthy, the inclusion of 2% CS produced better results than 1%. Overall, feeding C. gariepinus a diet supplemented with 2% CS significantly improved the fish's overall health, growth, and disease resistance, despite the ACR water pollution that consequently would sustain aquaculture.

Impact of indoor air pollution on the lung cancer – literature review

Introduction: Lung cancer is the most diagnosed type of cancer and the leading cause of death around the world. The most important risk factor for lung cancer is tobacco smoking. However, there are a lot of other lung cancer risk factors, which include: second-hand smoke exposure, environmental exposures (indoor and outdoor air pollution), occupational exposures, genetic predisposition, and previous lung disease. In this study, we would like to present the actual state of knowledge about the influence of radon as well as other indoor air pollutants on the prevalence of lung cancer.
 State of knowledge: We analyzed nineteen studies in terms of the impact of indoor air pollution on morbidity and mortality caused by lung cancer. The authors of the included studies agree that both radon and other household air pollution (HAP) increase risk of the lung cancer. HAPs are formed during the combustion of solid fuels (i.e. charcoal, wood). Indoor air pollution can cause in the lungs chronic inflammation, cells damage and their proliferation, depletion of antioxidants, impairment of defense mechanisms, production of reactive oxygen species as well as genetic mutations. Radon, on the other hand, emits alpha radiation, which can affect the respiratory epithelium and produce various cytotoxic and genotoxic effects, which promote carcinogenesis. The risk of lung cancer rises by approximately 6-16% per 100 Bq/m3 increase in long-time average residential radon concentration. 
 Conclusions: Radon and other indoor air pollutants are crucial lung cancer risk factors. It is essential to reduce HAPs production, especially in rural areas, where many people still use coal, wood, or straw for household heating and cooking. Moreover, there are regions where is a need to improve ventilation as well as to switch to clean fuel sources, such as gas and electricity. These activities will contribute to reducing the concentration of HAPs in buildings and decreasing the risk of lung cancer.

Long-term Performance of Conductive-backed multilayered HDPE Geomembranes

The long-term performance of three multilayered textured white conductive-backed geomembranes (GMBs) is compared to the comparable textured nonconductive GMBs and their smooth edge/equivalent to investigate the effect of the conductive layer on their longevity. Oven immersion in synthetic municipal solid waste leachate is used at a range of temperatures to accelerate the ageing during an incubation period of 50 months. It is shown that the conductive layer can antagonistically or synergistically affect the antioxidant depletion of conductive-backed GMBs relative to nonconductive GMBs produced by the same GMB manufacturer and formulated using the same nominal resin and antioxidant package. However, their relative degradation at 85 °C does not necessarily follow their relative antioxidant depletion times implying that the manufacturing process and the interaction between the additive packages of these GMBs can affect their relative degradation beyond the antioxidant depletion stage. Arrhenius modelling predicts the antioxidant depletion stage at field temperatures ranging between 180 and 1400 years at 20 °C for two different conductive-backed GMBs produced by two different manufacturers. With such variation in the long-term performance of conductive-backed GMBs currently available in the market, their durability should be investigated before their use in barrier systems to ensure they can meet the required design life of the desired geoenvironmental application.