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International Journal of Molecular... Jun 2024Increased fructose consumption and chronic stress, the major characteristics of modern lifestyle, impact human health; however, the consequences of their combination on...
Increased fructose consumption and chronic stress, the major characteristics of modern lifestyle, impact human health; however, the consequences of their combination on the uterus remain understudied. In this study, we investigated contractile activity, morphology, and intracellular activity of antioxidant enzymes in uteri from virgin Wistar rats subjected to liquid fructose supplementation and/or unpredictable stress over 9 weeks. Contractile activity and uterine response to oxytocin or adrenaline were examined using isolated bath chambers. Fructose supplementation, irrespective of stress, affected uterine morphology by increasing endometrium while decreasing myometrium volume density, attenuated uterine response to increasing doses of oxytocin, and increased glutathione peroxidase activity. Stress, irrespective of fructose, attenuated dose-dependent adrenaline-induced uterine relaxation. Stress, when applied solely, decreased mitochondrial superoxide dismutase activity. In the combined treatment, irregular estrous cycles and both reduced response to oxytocin and to adrenaline (as a consequence of fructose consumption and exposure to stress), along with fructose-related alteration of uterine morphology, were detected. In conclusion, fructose and stress affect uterine contractile activity, irrespective of each other, by inducing completely distinct responses in isolated uteri. In the combined treatment, the effects of both factors were evident, suggesting that the combination exerts more detrimental effects on the uterus than each factor individually.
Topics: Animals; Female; Fructose; Rats; Uterine Contraction; Rats, Wistar; Oxytocin; Uterus; Epinephrine; Stress, Physiological; Stress, Psychological; Superoxide Dismutase; Dietary Supplements; Myometrium; Antioxidants
PubMed: 38928475
DOI: 10.3390/ijms25126770 -
International Journal of Molecular... Jun 2024Water is a major requirement for our bodies, and alkaline water has induced an antioxidant response in a model of natural aging. A series of recent reports have shown...
Water is a major requirement for our bodies, and alkaline water has induced an antioxidant response in a model of natural aging. A series of recent reports have shown that aging is related to reduced water intake. Hydrogen-rich water has been suggested to exert a general antioxidant effect in relation to both improving lifestyle and preventing a series of diseases. Here, we wanted to investigate the effect of the daily intake of hydrogen-rich alkaline water (HAW) in counteracting the redox imbalance induced in a model of HO-treated mice. Mice were treated with HO for two weeks and either left untreated or supplied with HAW. The results show that HAW induced a reduction in the ROS plasmatic levels that was consistent with the increase in the circulating glutathione. At the same time, the reduction in plasmatic 8-hydroxy-2'-deoxyguanosine was associated with reduced DNA damage in the whole body. Further analysis of the spleen and bone marrow cells showed a reduced ROS content consistent with a significantly reduced mitochondrial membrane potential and superoxide accumulation and an increase in spontaneous proliferation. This study provides evidence for a clear preventive and curative effect of HAW in a condition of systemic toxic condition and redox imbalance.
Topics: Animals; Mice; Hydrogen Peroxide; Hydrogen; Oxidation-Reduction; Reactive Oxygen Species; Water; Oxidative Stress; Antioxidants; DNA Damage; Male; Membrane Potential, Mitochondrial; 8-Hydroxy-2'-Deoxyguanosine; Glutathione; Dietary Supplements
PubMed: 38928440
DOI: 10.3390/ijms25126736 -
International Journal of Molecular... Jun 2024A homozygous mutation of the gene causes autosomal recessive familial type 19 of Parkinson's disease (PARK19). To test the hypothesis that PARK19 DNAJC6 mutations...
A homozygous mutation of the gene causes autosomal recessive familial type 19 of Parkinson's disease (PARK19). To test the hypothesis that PARK19 DNAJC6 mutations induce the neurodegeneration of dopaminergic cells by reducing the protein expression of functional DNAJC6 and causing DNAJC6 paucity, an in vitro PARK19 model was constructed by using shRNA-mediated gene silencing of endogenous DANJC6 in differentiated human SH-SY5Y dopaminergic neurons. shRNA targeting DNAJC6 induced the neurodegeneration of dopaminergic cells. DNAJC6 paucity reduced the level of cytosolic clathrin heavy chain and the number of lysosomes in dopaminergic neurons. A DNAJC6 paucity-induced reduction in the lysosomal number downregulated the protein level of lysosomal protease cathepsin D and impaired macroautophagy, resulting in the upregulation of pathologic α-synuclein or phospho-α-synuclein in the endoplasmic reticulum (ER) and mitochondria. The expression of α-synuclein shRNA or cathepsin D blocked the DNAJC6 deficiency-evoked degeneration of dopaminergic cells. An increase in ER α-synuclein or phospho-α-synuclein caused by DNAJC6 paucity activated ER stress, the unfolded protein response and ER stress-triggered apoptotic signaling. The lack of DNAJC6-induced upregulation of mitochondrial α-synuclein depolarized the mitochondrial membrane potential and elevated the mitochondrial level of superoxide. The DNAJC6 paucity-evoked ER stress-related apoptotic cascade, mitochondrial malfunction and oxidative stress induced the degeneration of dopaminergic neurons via activating mitochondrial pro-apoptotic signaling. In contrast with the neuroprotective function of WT DNAJC6, the PARK19 DNAJC6 mutants (Q789X or R927G) failed to attenuate the tunicamycin- or rotenone-induced upregulation of pathologic α-synuclein and stimulation of apoptotic signaling. Our data suggest that PARK19 mutation-induced DNAJC6 paucity causes the degeneration of dopaminergic neurons via downregulating protease cathepsin D and upregulating neurotoxic α-synuclein. Our results also indicate that PARK19 mutation (Q789X or R927G) impairs the DNAJC6-mediated neuroprotective function.
Topics: Cathepsin D; Dopaminergic Neurons; Humans; alpha-Synuclein; HSP40 Heat-Shock Proteins; Endoplasmic Reticulum Stress; Up-Regulation; Parkinson Disease; Mitochondria; Lysosomes; Down-Regulation; Apoptosis; Cell Line, Tumor
PubMed: 38928416
DOI: 10.3390/ijms25126711 -
International Journal of Molecular... Jun 2024Polyurethane/silk protein-bismuth halide oxide composite films were fabricated using a blending-wet phase transformationin situsynthesis method. The crystal structure,...
Polyurethane/silk protein-bismuth halide oxide composite films were fabricated using a blending-wet phase transformationin situsynthesis method. The crystal structure, micromorphology, and optical properties were conducted using XRD, SEM, and UV-Vis DRS characterize techniques. The results indicated that loaded silk protein enhanced the hydrophilicity and pore structure of the polyurethane composite films. The active species BiOX were observed to grow as nanosheets with high dispersion on the internal skeleton and silk protein surface of the polyurethane-silk protein film. The photocatalytic efficiency of BiOX/PU-SF composite films was assessed through the degradation of Rhodamine B under visible light irradiation. Among the tested films, the BiOBr/PU-SF composite exhibited the highest removal rate of RhB at 98.9%, surpassing the removal rates of 93.7% for the BiOCl/PU-SF composite and 85.6% for the BiOI/PU-SF composite. Furthermore, an active species capture test indicated that superoxide radical (•O) and hole (h) species played a predominant role in the photodegradation process.
Topics: Polyurethanes; Photolysis; Hydrophobic and Hydrophilic Interactions; Bismuth; Catalysis; Silk; Rhodamines; Coloring Agents; Oxides; Porosity; Light
PubMed: 38928359
DOI: 10.3390/ijms25126653 -
International Journal of Molecular... Jun 2024Hydrogen sulfide (HS) is a novel gasotransmitter. Sucrose (SUC) is a source of cellular energy and a signaling molecule. Maize is the third most common food crop...
Hydrogen sulfide (HS) is a novel gasotransmitter. Sucrose (SUC) is a source of cellular energy and a signaling molecule. Maize is the third most common food crop worldwide. However, the interaction of HS and SUC in maize thermotolerance is not widely known. In this study, using maize seedlings as materials, the metabolic and functional interactions of HS and SUC in maize thermotolerance were investigated. The data show that under heat stress, the survival rate and tissue viability were increased by exogenous SUC, while the malondialdehyde content and electrolyte leakage were reduced by SUC, indicating SUC could increase maize thermotolerance. Also, SUC-promoted thermotolerance was enhanced by HS, while separately weakened by an inhibitor (propargylglycine) and a scavenger (hypotaurine) of HS and a SUC-transport inhibitor (N-ethylmaleimide), suggesting the interaction of HS and SUC in the development of maize thermotolerance. To establish the underlying mechanism of HS-SUC interaction-promoted thermotolerance, redox parameters in mesocotyls of maize seedlings were measured before and after heat stress. The data indicate that the activity and gene expression of HS-metabolizing enzymes were up-regulated by SUC, whereas HS had no significant effect on the activity and gene expression of SUC-metabolizing enzymes. In addition, the activity and gene expression of catalase, glutathione reductase, ascorbate peroxidase, peroxidase, dehydroascorbate reductase, monodehydroascorbate reductase, and superoxide dismutase were reinforced by HS, SUC, and their combination under non-heat and heat conditions to varying degrees. Similarly, the content of ascorbic acid, flavone, carotenoid, and polyphenol was increased by HS, SUC, and their combination, whereas the production of superoxide radicals and the hydrogen peroxide level were impaired by these treatments to different extents. These results imply that the metabolic and functional interactions of HS and sucrose signaling exist in the formation of maize thermotolerance through redox homeodynamics. This finding lays the theoretical basis for developing climate-resistant maize crops and improving food security.
Topics: Zea mays; Hydrogen Sulfide; Oxidation-Reduction; Thermotolerance; Sucrose; Gene Expression Regulation, Plant; Heat-Shock Response; Seedlings; Plant Proteins
PubMed: 38928304
DOI: 10.3390/ijms25126598 -
Genes Jun 2024Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease targeting the brain and spinal cord. Non-neuronal cells, including macrophages, may contribute to the...
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease targeting the brain and spinal cord. Non-neuronal cells, including macrophages, may contribute to the disruption of motor neurons (MNs), neuromuscular junction dismantling and clinical signs of ALS. Understanding the modality and the effect of MNs-macrophage communication is pivotal. Here, we focus on extracellular vesicle (EVS)-mediated communication and, in particular, we analyze the response of macrophages. NSC-34 cells transfected with mutant SOD1 (G93A, A4V, G85R, G37R) and differentiated towards MN-like cells, and Raw 264.7 macrophages are the cellular models of the study. mSOD1 NSC-34 cells release a high number of vesicles, both large-lEVs (300 nm diameter) and small-sEVs (90 nm diameter), containing inflammation-modulating molecules, and are efficiently taken up by macrophages. RT-PCR analysis of inflammation mediators demonstrated that the conditioned medium of mSOD1 NSC-34 cells polarizes Raw 264.7 macrophages towards both pro-inflammatory and anti-inflammatory phenotypes. sEVs act on macrophages in a time-dependent manner: an anti-inflammatory response mediated by TGFβ firstly starts (12 h); successively, the response shifts towards a pro-inflammation IL-1β-mediated (48 h). The response of macrophages is strictly dependent on the SOD1 mutation type. The results suggest that EVs impact physiological and behavioral macrophage processes and are of potential relevance to MN degeneration.
Topics: Animals; Extracellular Vesicles; Mice; RAW 264.7 Cells; Superoxide Dismutase-1; Macrophages; Amyotrophic Lateral Sclerosis; Motor Neurons; Inflammation; Mutation; Transfection; Humans
PubMed: 38927671
DOI: 10.3390/genes15060735 -
Biomedicines May 2024The escalating rates of morbidity and mortality associated with opioid use disorder (OUD) have spurred a critical need for improved treatment outcomes. This study aimed...
The escalating rates of morbidity and mortality associated with opioid use disorder (OUD) have spurred a critical need for improved treatment outcomes. This study aimed to investigate the impact of prolonged exposure to Fentanyl, a potent opioid, on behavior, biochemical markers, oxidative stress, and the composition of the gut microbiome. Additionally, we sought to explore the therapeutic potential of in mitigating the adverse effects of Fentanyl withdrawal. The study unveiled that chronic Fentanyl administration induced a withdrawal syndrome characterized by elevated cortisol levels (12.09 mg/mL, compared to 6.3 mg/mL for the control group). This was accompanied by heightened anxiety, indicated by a reduction in time spent and entries made into the open arm in the Elevated Plus Maze Test, as well as depressive-like behaviors, manifested through increased immobility time in the Forced Swim Test. Additionally, Fentanyl exposure correlated with decreased gut microbiome density and diversity, coupled with heightened oxidative stress levels, evidenced by elevated malondialdehyde (MDA) and reduced levels of catalase (CAT) and superoxide dismutase (SOD). However, both post- and co-administration of exhibited substantial improvements in these adverse effects, effectively alleviating symptoms associated with OUD withdrawal syndrome and eliciting positive influences on gut microbiota. In conclusion, this research underscores the therapeutic potential of in managing Fentanyl withdrawal symptoms. The findings indicate promising effects in alleviating behavioral impairments, reducing stress, restoring gut microbiota, and mitigating oxidative stress, offering valuable insights for addressing the challenges of OUD treatment.
PubMed: 38927359
DOI: 10.3390/biomedicines12061152 -
Biology Jun 2024The prevalence of waterpipe tobacco smoking (WPS) is increasing worldwide and is relatively high among youth and young adults. It has been shown, both experimentally and...
The prevalence of waterpipe tobacco smoking (WPS) is increasing worldwide and is relatively high among youth and young adults. It has been shown, both experimentally and clinically, that WPS exposure adversely affects the cardiovascular and hematological systems through the generation of oxidative stress and inflammation. Our study aimed to evaluate the impact of WPS exposure on erythrocytes, a major component of the hematological system, of BALB/c mice. Here, we assessed the effect of nose-only WPS exposure for four consecutive weeks on erythrocyte inflammation, oxidative stress, and eryptosis. The duration of the session was 30 min/day, 5 days/week. Control mice were exposed to air. Our results showed that the levels of C-reactive protein, lipid peroxidation (LPO), superoxide dismutase, and total nitric oxide (NO) were significantly increased in the plasma of WPS-exposed mice. The number of erythrocytes and the hematocrit were significantly decreased in WPS-exposed mice compared with the control group. Moreover, there was an increase in the erythrocyte fragility in mice exposed to WPS compared with those exposed to air. The levels of lactate dehydrogenase, LPO, reduced glutathione, catalase, and NO were significantly increased in the red blood cells (RBCs) of WPS-exposed mice. In addition, erythrocytes of the WPS-exposed group showed a significant increase in ATPase activity, Ca, annexin V binding, and calpain activity. Taken together, our findings suggest that WPS exposure elevated inflammation and oxidative stress in the plasma and induced hemolysis in vivo. It also caused alterations of RBCs oxidative stress and eryptosis in vitro. Our data confirm the detrimental impact of WPS on erythrocyte physiology.
PubMed: 38927333
DOI: 10.3390/biology13060453 -
Biology Jun 2024Canola is the largest self-produced vegetable oil source in China, although excessive levels of cadmium, lead, and arsenic seriously affect its yield. Therefore,...
Canola is the largest self-produced vegetable oil source in China, although excessive levels of cadmium, lead, and arsenic seriously affect its yield. Therefore, developing methods to identify canola materials with good heavy metal tolerance is a hot topic for canola breeding. In this study, canola near-isogenic lines with different oil contents (F338 (40.62%) and F335 (46.68%) as the control) and heavy metal tolerances were used as raw materials. In an experiment with 100 times the safe standard values, the superoxide dismutase (SOD) and peroxidase (POD) activities of F335 were 32.02 mmol/mg and 71.84 mmol/mg, while the activities of F338 were 24.85 mmol/mg and 63.86 mmol/mg, exhibiting significant differences. The DEGs and DAPs in the MAPK signaling pathway of the plant hormone signal transduction pathway and other related pathways were analyzed and verified using RT-qPCR. SAUR36 and SAUR32 were identified as the key differential genes. The expression of the SAUR36 gene in canola materials planted in the experimental field was significantly higher than in the control, and FY958 exhibited the largest difference (27.82 times). In this study, SOD and SAUR36 were found to be closely related to heavy metal stress tolerance. Therefore, they may be used to screen for new canola materials with good heavy metal stress tolerance for canola breeding.
PubMed: 38927321
DOI: 10.3390/biology13060441 -
Biology May 2024The purpose of this study was to explore the effects of Res and EGCG on cell growth, cellular antioxidant levels, and cellular lipid metabolism in hepatocytes. In this...
The purpose of this study was to explore the effects of Res and EGCG on cell growth, cellular antioxidant levels, and cellular lipid metabolism in hepatocytes. In this experiment, leghorn male hepatoma (LMH) cells were used as hepatocytes. The results showed that 6.25-25 μM Res and EGCG had no adverse effects on cell viability and growth. Meanwhile, with the increasing dosage of Res and EGCG, the contents of total cholesterol (TC), total glyceride (TG), and malondialdehyde (MDA) in hepatocytes decreased significantly ( < 0.05), while the contents of glutathione peroxidase (GSH-Px), total superoxide dismutase (T-SOD), and catalase (CAT) increased significantly ( < 0.05). In addition, western blot results showed that Res and EGCG could significantly increase the expression of p-AMPK protein and reduce the expression of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) protein in hepatocytes ( < 0.05). Moreover, q-PCR results showed that with the increase in Res and EGCG, the expression of cholesterol- and fatty acid synthesis-related genes decreased significantly ( < 0.05). In conclusion, Res and EGCG can increase the antioxidant capacity of hepatocytes and reduce the synthesis of TC and TG in hepatocytes by activating AMPK, thereby regulating lipid metabolism in hepatocytes.
PubMed: 38927248
DOI: 10.3390/biology13060368