Increased MDA Content Research Articles

Monitoring of potato viruses in the Altai region and their influence on morphometric and biochemical parameters of plants

Potatoes are one of the most important food crops, and most susceptible to diseases, including viral ones. They can lead to significant yield losses (up to 30-80 %), and in the case of infection by several viruses, this damage increases. The article presents the results of evaluation of viral infection of seed potatoes in Altai Territory (10 potato samples from Kytmanovsky, Pervomaisky districts and Barnaul city) and its influence on morphometric and biochemical parameters of plants. The presence of viruses (X, Y, M, A, S, leafroll virus and tuber spindle viroid) in the samples was determined by RT-PCR using a ‘SINTOL’ set of reagents. Biochemical parameters: chlorophyll a and b concentrations, malonic dialdehyde, peroxidase activity were determined spectrophotometrically. The maximum frequency of occurrence in the districts of the region was observed for two viruses PVY, PVS. On varieties Colomba and Juwel, the prevalence of Y virus reached 100 %, S virus 90-100 %. Tuber spindle viroid (quarantine object), leafroll virus and A virus were absent in all tested samples. Evaluation of morphometric indices revealed a 1.4-fold decrease in the number of leaves affected by virus Y, relative to virus-free plants (variety Colombo). On the variety Gala, the combination of Y+S viruses caused in plants a reduction of leaf plates and an increase in the number of leaves by 1.9 times. S virus infection of Gala variety resulted in a 1.27-fold increase in MDA concentration and a 1.26-fold increase in peroxidase activity. Combined virus infection (PVY + PVS) enhanced the negative effect observed with mono-infection.

Temperature-dependent toxicity and mechanisms of florfenicol on the embryonic development of marine medaka (Oryzias melastigma).

The extensive use of antibiotics and their persistence in the environment have seriously threatened marine ecosystems in recent years. The frequent occurrence of extreme weather due to climate change has also increased the uncertainty of effective toxicity identification and risk assessment of the chemicals of concern. This study aimed to investigate the toxic effects and potential mechanisms of florfenicol (0.5, 10, 100, 500 and 1000 μg/L) on the embryonic development of marine medaka (Oryzias melastigma) through 21-d experiment under three temperature exposure scenarios (20, 25, and 30 °C). Considering embryo development, the highest level of florfenicol at 1000 μg/L decreased the hatching success at 25 °C, whereas the total inhibition of hatching was observed at 20 °C regardless of florfenicol concentrations of concern. The ATP content was inhibited by the highest florfenicol dose at 20 °C, while stimulated ATP content at 20 °C and 30 °C, compared to 25 °C. Fluctuation of temperatures, especially at 20 ℃, induced oxidative stresses, including increased MDA contents and decreased CYP450 and HSP90 contents. For inflammatory response-related genes (nf-κb, nlrx1, pycard, caspase 1, and il-1β), an increase of florfenicol dose led to gene upregulation at 25 °C. Conversely, gene upregulation was also observed for all treatments at 30 °C, while predominantly downregulation was observed for all treatments at 20 °C. For genes related to DNA damage and apoptosis (pi3k, akt, foxo1, tp53, bcl-2, bax, apaf-1, caspase 9, and 3), alterations in gene expression were evident for all florfenicol treatments at both 20 °C and 30 °C. Therefore, this study suggests that the combined effects of florfenicol and temperature may disrupt the normal function of mitochondria, impacting ATP production, thereby inducing oxidative stress, inflammatory response, DNA damage, and apoptosis, ultimately resulting in decreased hatching rates and increased mortality. Furthermore, the key findings of this study reveal the complex interactions between florfenicol and temperature and emphasize the need to consider temperature when identifying toxicity and mechanisms, as well as the ecological risk assessment of florfenicol in marine environments.

Entacapone alleviates muscle atrophy by modulating oxidative stress, proteolysis, and lipid aggregation in multiple mice models

BackgroundSkeletal muscle atrophy significantly affects quality of life and has socio-economic and health implications. This study evaluates the effects of entacapone (ENT) on skeletal muscle atrophy linked with oxidative stress and proteolysis.MethodsC2C12 cells were treated with dexamethasone (Dex) to simulate muscle atrophy. Four murine models were employed: diaphragm atrophy from mechanical ventilation, Dex-induced atrophy, lipopolysaccharide (LPS)-induced atrophy, and hyperlipidemia-induced atrophy. Each model utilized entacapone (10 mg/kg), with sample sizes: Control (9), MV (11), MV + ENT (5) for diaphragm atrophy; Control (4), Dex (4), Dex + ENT (5) for Dex model; Control (4), LPS (4), LPS + ENT (5) for LPS model; and similar for hyperlipidemia. Measurements included muscle strength, myofiber cross-sectional area (CSA), proteolysis, oxidative stress markers [uperoxide dismutase 1 (SOD1), uperoxide dismutase 2 (SOD2), 4-hydroxynonenal (4-HNE)], and lipid levels.ResultsOur findings confirm Dex-induced muscle atrophy, evidenced by increased expression of muscle atrophy-associated proteins, including Atrogin-1 and Murf-1, along with decreased diameter of C2C12 myotubes. Atrogin-1 levels rose by 660.6% (p < 0.05) in the Dex group compared to control, while entacapone reduced Atrogin-1 by 84.4% (p < 0.05). Similarly, Murf-1 levels increased by 365% (p < 0.05) in the Dex group and were decreased by 89.5% (p < 0.05) with entacapone. Dexamethasone exposure induces oxidative stress, evidenced by the upregulation of oxidative stress-related proteins Sod1, Sod2, and 4-HNE. Entacapone significantly reduced the levels of these oxidative stress markers, enhancing GSH-PX content by 385.6% (p < 0.05) compared to the Dex-treated group. Additionally, ENT effectively reduced the Dex-induced increase in MDA content by 63.98% (p < 0.05). Furthermore, entacapone effectively prevents the decline in diaphragm muscle strength and myofiber CSA in mice. It also mitigates diaphragm oxidative stress and protein hydrolysis. Additionally, entacapone exhibits the ability to attenuate lipid accumulation in the gastrocnemius muscle of hyperlipidemic mice and alleviate the reduction in muscle fiber CSA.ConclusionOur findings suggest that entacapone is a promising therapeutic candidate for muscle atrophy, functioning through the reduction of oxidative stress, proteolysis, and lipid aggregation. Future research should explore the underlying mechanisms and potential clinical applications of entacapone in muscle-wasting conditions.

An integrated physiological indicator and transcriptomic analysis reveals the response of soybean buds to high-temperature stress.

Under global warming, high temperature (HT) has become a major meteorological factor affecting soybean production. To explore the candidate genes and regulatory mechanism of the soybean bud response to HT stress, previously identified as HT-tolerant ('Handou14'; HD14) and HT-sensitive ('Jiadou36'; JD36) were treated for 5 days in an artificial climate incubator either with HT (43°C (day)/ 33°C (night), 16h light/8h darkness) or the non-stress growth condition (25°C, 16h light/8h darkness) as the control at the bud stage were used as experimental materials in this study. After HT treatment, changes in physiological indicators including hypocotyl length, enzyme activity and hormone content were detected; at the same time, the cotyledons, hypocotyls, and main roots were collected for transcriptome sequencing analysis. Analyzing the mechanisms of HT stress response in the bud stage of HD14 and JD36 at physiological and transcription levels. Analysis of physiological indicator showed that the activities of superoxide dismutase (SOD) were significantly increased 47.4% and 41.2% in the cotyledon of HD14 and the main root of JD36, and the contents of peroxidase (POD) were significantly increased 61.5% and 125% in the hypocotyl of HD14 and JD36; the contents of malonaldehyde (MDA) were significantly increased 44.8% and 22.2% in the main root of HD14 and JD36 after HT treatment. The content of abscisic acid (ABA) were significantly increased 1.9 fold and 1.2 fold in the root of HD14 and JD36 in response to HT treatment, whereas the content of gibberellin (GA) were decreased 2.2 fold and 1.3 fold in the cotyledon and root, and increased 1.6 fold in the hypocotyl in HD14 (P < 0.05). Thus, higher SOD and POD activities, higher ABA content, and a smaller increase in MDA content may improve tolerance to HT stress. The HT-tolerant cultivar may have stronger GA signal transduction in the hypocotyl to combat the negative effects of HT. RNA-sequencing was performed to analyze the differential expression of genes in buds of the two cultivars under the HT treatment and control condition. In total, 3,633, 1,964, 9,934, and 3,036 differentially expressed genes (DEGs) were identified in the CH (control group of HD14) vs. TH (HT-treatment group of HD14), CJ (control group of JD36) vs. TJ (HT-treatment group of JD36), TJ vs. TH, and CJ vs. CH comparison groups, respectively. Bioinformatic analysis revealed that most DEGs were mainly involved in metabolic processes, catalytic activity, carbohydrate, energy transduction, and signaling pathways. The results of qRT-PCR validation (86.67%) and changes in physiological indicators were consistent with the RNA-sequencing data. Five DEGs were selected as candidate genes in the response to HT stress at the bud stage. In summary, soybean cells are protected from oxidative damage by an increase in antioxidant enzyme activities and accumulation of hormone content under HT stress. Concomitantly, changes in the expression of crucial genes and signal transmission processes are induced, thus initiating adaptive and protective mechanisms. This study provides a theoretical basis for clarification of the physiological and molecular mechanisms in the response to HT stress of soybean bud.

Ethyl gallate ameliorates diabetes-induced Alzheimer's disease-like phenotype in rats via activation of α7 nicotinic receptors and mitigation of oxidative stress

Cognitive decline, an important comorbidity of type 2 diabetes (T2D), is attributed to oxidative stress and impaired cholinergic signaling in the brain. The α7 nicotinic acetylcholine receptor (α7nAChR) is densely distributed in the hippocampus and cortex, and exerts neuroprotective and procognitive actions. Ethyl gallate (EG), a natural phenolic antioxidant compound, showed high in-silico binding affinity towards α7nAChR and brain penetrability. Therefore, the present study aimed to evaluate the involvement of α7nAChR in the potential of EG to ameliorate T2D-induced Alzheimer's disease-like condition. T2D was induced by intraperitoneal (i.p.) injection of streptozotocin (35 mg/kg) in rats on high-fat diet. Diabetic animals were treated with EG (10 and 20 mg/kg, i.p.) for four weeks, and their learning and memory performance was evaluated by the Morris water maze (MWM). Further, the brains were subjected to biochemical analysis of antioxidants like glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT), and oxidative stress marker malonaldehyde (MDA). While diabetic rats showed a significant decline in cognitive performance in the MWM, a substantial improvement was noticed following EG treatment. Further, the diabetes-associated reductions in GSH, SOD, and CAT levels, along with increased MDA contents in the brain, were effectively restored by EG. Interestingly, pre-treatment with α7nAChR antagonist methyllycaconitine (1 mg/kg, i.p.) attenuated the effects of EG on behavioral and biochemical parameters. The results suggest that EG may augment cholinergic signaling in the brain via α7nAChR to mitigate oxidative stress, consequently alleviating T2D-associated dementia. Therefore, EG could be a potential candidate for addressing cognitive impairment comorbid with T2D.

Deoxynivalenol-mediated kidney injury via endoplasmic reticulum stress in mice

ObjectiveDeoxynivalenol (DON) is a common fungal toxin that poses significant health risks to humans and animals. The present study aimed to investigate the adverse effects and molecular mechanisms of DON-induced kidney injury. MethodsMale C57BL/6 mice aged 5–6 weeks were used to establish a DON-induced acute kidney injury model. Histological analysis, biochemical assays, molecular techniques, Western blot, RNA sequencing, and transmission electron microscopy were employed to analyze kidney damage, inflammation, oxidative stress, apoptosis, and endoplasmic reticulum (ER) stress. ResultsDON disrupted kidney morphology, induced inflammatory cell infiltration, and triggered inflammatory responses. DON increased MDA content while decreasing antioxidant enzyme activity (SOD and CAT). It also triggered apoptosis, evidenced by elevated levels of caspase-12, cleaved caspase-3, and BAX, and reduced levels of Bcl-2. Transcriptomic analysis identified distinct expression patterns in 1756 genes in DON-exposed mouse kidneys, notably upregulating ER stress-related genes. Further investigation revealed ultrastructural changes in the ER and mitochondrial damage induced by DON, along with increased levels of p-IRE1, p-PERK, and their downstream targets, indicating unfolded protein response (UPR) activation in the kidney. The ER stress inhibitor 4-Phenylbutyric acid (4-PBA) significantly mitigated DON-induced ER stress, oxidative damage, apoptosis, tissue injury, ER expansion, and mitochondrial damage. ConclusionOur findings highlight the role of ER stress in DON-induced kidney injury and the protective effect of 4-PBA against these adverse effects.

Biocontrol of Fusarium oxysporum-infested Gastrodia elata Bl. by Lactobacillus curvatus 2768-VOCs and mechanism of inhibition

Gastrodia elata Bl. Is susceptible to infestation by the fungus Fusarium oxysporum, which can cause severe post-harvest diseases. This paper presents the findings of an investigation into the control and bacteriostatic mechanisms of Lactobacillus curvatus 2768-VOCs on F. oxysporum-infected G. elata. The results of both in vitro and in vivo tests demonstrated that L. curvatus 2768-VOCs exhibited inhibitory effects against F. oxysporum, with inhibition rates of 63.37% and 44.4%, respectively. The results of the in vivo test also demonstrated that the pre-fumigation approach exhibited superior efficacy compared to direct fumigation, with the former showing a preventive effect. Furthermore, it was discovered that VOCs disrupted the integrity of F. oxysporum cell membranes and altered their permeability, resulting in the leakage of cell contents. The fumigation caused damage to the mycelial structure, accompanied by a notable decline in the total lipid and ergosterol content, and an appreciable increase in MDA content. Moreover, the fumigation of VOCs markedly diminished the activities of ATPase and mitochondrial dehydrogenase, thereby disrupting the respiration of F. oxysporum and its energy metabolism. The VOCs were subjected to GC-MS analysis, which revealed that the relative content of acids was the highest, particularly formic acid and glyoxalic acid. The study offers a theoretical basis for the biological control of postharvest diseases in G. elata.

Thermal-induced interactions between soy protein isolate and malondialdehyde: Effects on protein digestibility, structure, and formation of advanced lipoxidation end products

Thermally processed lipid- and protein-rich foods have sparked widespread concern since they may degrade food nutrition and even risk food safety. This study investigated soy protein isolate (SPI) alterations of digestibility and structure, as well as the formation of potentially hazardous chemicals, i.e., advanced lipoxidation end products (ALEs), after interacting with malondialdehyde (MDA, a lipid oxidation product) under high-temperature cooking conditions (100–180 °C, up to 60 min). In-vitro protein digestion of the SPI-MDA mixtures suggested that their room-temperature interactions damaged SPI digestibility, and increasing the temperature and the duration of the thermal treatment exacerbated the adverse effects. Protein oxidation, covalent aggregation of subunits, and changes in secondary and tertiary structures were revealed using thiol quantification, gel electrophoresis, fluorescence spectroscopy, and circular dichroism (CD) spectra, which could explain reduced protein digestibility. High-resolution mass spectrometry (HRMS) identified seven non-crosslinked ALEs and two crosslinked ALEs. Increased MDA concentrations promoted the generation of ALEs. Moreover, the acrolein-derived ALEs with reactive carbonyl groups were prone to further reacting into crosslinked ALEs, potentially responsible for the subunit aggregation.

Physiological Responses and Quality Alterations of Pea Sprouts under Salt Stress: Implications for Salt-Tolerant Mechanism

Pea sprouts, considered a nutritious and environmentally sustainable vegetable with significant cultivation prospects and market potential, face growth challenges due to salt stress. However, the underlying mechanisms associated with this stress have not been fully elucidated. To address this knowledge gap, we conducted a hydroponic study applying various concentrations of NaCl salt stress to pea sprouts. Systematic analysis was performed on key parameters including germination, plant height, biomass, and enzyme activity of pea sprouts under salt treatment. Our aim was to unravel the underlying mechanisms associated with the impact of salt stress on the growth of pea sprouts. Results revealed that salt treatment significantly inhibited the germination process of pea sprouts’ seeds, leading to a notable decrease in plant height and sprout yield. Salt stress induced an increase in MDA content, a decrease in chlorophyll content, and elevated relative conductivity. However, a low concentration of salt treatment enhanced SOD activity, suggesting the activation of oxidative stress resistance mechanisms in pea sprouts. Moreover, salt treatment exhibited an inhibitory effect on soluble protein content while promoting soluble sugar content in pea sprouts. Additionally, low-concentration salt treatment increased the crude fiber content of pea sprouts, while high-concentration salt treatment inhibited it. In summary, this study indicates that salt stress could cause physiological damage to pea sprouts, but pea sprouts may employ metabolic strategies to adapt to the low concentration of salt stress. These findings contribute to a deeper understanding of the physiological responses of pea sprouts to salt stress and provide valuable insights for its implementation of salt-tolerant cultivation.

Pseudochrobactrum asaccharolyticum mitigates arsenic induced oxidative stress of maize plant by enhancing water status and antioxidant defense system

BackgroundOxidative stress mediated by reactive oxygen species (ROS) is a common denominator in arsenic toxicity. Arsenic stress in soil affects the water absorption, decrease stomatal conductance, reduction in osmotic, and leaf water potential, which restrict water uptake and osmotic stress in plants. Arsenic-induced osmotic stress triggers the overproduction of ROS, which causes a number of germination, physiological, biochemical, and antioxidant alterations. Antioxidants with potential to reduce ROS levels ameliorate the arsenic-induced lesions. Plant growth promoting rhizobacteria (PGPR) increase the total soluble sugars and proline, which scavenging OH radicals thereby prevent the oxidative damages cause by ROS. The main objective of this study was to evaluate the potential role of Arsenic resistant PGPR in growth of maize by mitigating arsenic stress.MethodologyArsenic tolerant PGPR strain MD3 (Pseudochrobactrum asaccharolyticum) was used to dismiss the ‘As’ induced oxidative stress in maize grown at concentrations of 50 and 100 mg/kg. Previously isolated arsenic tolerant bacterial strain MD3 “Pseudochrobactrum asaccharolyticum was used for this experiment. Further, growth promoting potential of MD3 was done by germination and physio-biochemical analysis of maize seeds. Experimental units were arranged in Completely Randomized Design (CRD). A total of 6 sets of treatments viz., control, arsenic treated (50 & 100 mg/kg), bacterial inoculated (MD3), and arsenic stress plus bacterial inoculated with three replicates were used for Petri plates and pot experiments. After treating with this MD3 strain, seeds of corn were grown in pots filled with or without 50 mg/kg and 100 mg/kg sodium arsenate.ResultsThe plants under arsenic stress (100 mg/kg) decreased the osmotic potential (0.8 MPa) as compared to control indicated the osmotic stress, which caused the reduction in growth, physiological parameters, proline accumulation, alteration in antioxidant enzymes (Superoxide dismutase-SOD, catalase-CAT, peroxidase-POD), increased MDA content, and H2O2 in maize plants. As-tolerant Pseudochrobactrum asaccharolyticum improved the plant growth by reducing the oxidation stress and antioxidant enzymes by proline accumulation. PCA analysis revealed that all six treatments scattered differently across the PC1 and PC2, having 85.51% and 9.72% data variance, respectively. This indicating the efficiency of As-tolerant strains. The heatmap supported the As-tolerant strains were positively correlated with growth parameters and physiological activities of the maize plants.ConclusionThis study concluded that Pseudochrobactrum asaccharolyticum reduced the ‘As’ toxicity in maize plant through the augmentation of the antioxidant defense system. Thus, MD3 (Pseudochrobactrum asaccharolyticum) strain can be considered as bio-fertilizer.

Response to Hyperthermia and Hypoxia Stress during Compensatory Growth in Penaeus vannamei

This study evaluated oxidative stress and resistance to abiotic stress factors of juvenile Penaeus vannamei during compensatory growth. Shrimp underwent two dietary treatments in a 50-day experiment: a reference group (REF) fed ad libitum and a restricted group (T50) fed 50% of the REF diet for 10 days, followed by 40 days of ad libitum refeeding. During refeeding, shrimp from both groups were exposed to two abiotic challenges: 1) hyperthermia (34°C) for 12 hours and 2) hypoxia (1.5 mgO2 L-1) for 9 hours, followed by reoxygenation for 3 hours (5 mgO2 L-1). Compensatory growth in the T50 group was evidenced by increased specific growth rate, hyperphagia, and improved feed efficiency. Moreover, the malondialdehyde content (MDA) and catalase activity in the shrimp hepatopancreas increased during compensatory growth, indicating oxidative stress. This result converges with the increased metabolism assessed by metabolic chambers. While hyperthermia caused oxidative stress, as indicated by the increase in MDA content in both groups, shrimp under compensatory growth demonstrated similar resistance to the REF group. Exposition to hypoxia and reoxygenation did not generate significant oxidative stress. Compensatory growth induced oxidative stress in P. vannamei without compromising resistance to hyperthermia or hypoxia events.

Changes in the Morphology and Antioxidant Status of European Red Deer Sperm Stored in the Epididymides and in a Liquid State.

The aim of this study was to evaluate the motility, morphology, and antioxidant status of European red deer sperm stored in a liquid state (variant I) and in the epididymides (variant II). Spermatozoa were harvested post-mortem from the cauda epididymis. Sperm samples in both variants were stored for up to six days (D6) at 5 °C. Spermatozoa were assessed for motility, viability, morphology, activity of antioxidant enzymes (superoxide dismutase, SOD; glutathione peroxidase, GPx; catalase, CAT), and lipid peroxidation (malondialdehyde, MDA, content). Sperm samples were analyzed on storage days 0, 2, 4, and 6 (D0-D6). Storage time and storage method significantly (p ≤ 0.05) influenced the examined variables. On D2, a decrease in motility and acrosomal integrity was observed in both storage variants, whereas a decrease in viability and an increase in MDA content were noted in spermatozoa stored in the epididymides. On D4, higher values of SOD and GPx activity and MDA content were noted in variant I than in variant II. Catalase activity was very low. GPx is the key enzyme that participates in the reduction of hydrogen peroxide in sperm cells. Spermatozoa stored in a liquid state were characterized by higher motility and viability, improved morphology and antioxidant status than those stored in the epididymides; therefore, liquid storage is more recommended for short-term preservation of epididymal spermatozoa.

Huperzine A ameliorates neurological deficits after spontaneous subarachnoid hemorrhage through endothelial cell pyroptosis inhibition.

Spontaneous subarachnoid hemorrhage (SAH) is a kind of hemorrhagic stroke which causes neurological deficits in survivors. Huperzine A has a neuroprotective effect, but its role in SAH is unclear. Therefore, we explore the effect of Huperzine A on neurological deficits induced by SAH and the related mechanism. In this study, Evans blue assay, TUNEL staining, immunofluorescence, western blot analysis, and ELISA are conducted. We find that Huperzine A can improve neurological deficits and inhibit the apoptosis of nerve cells in SAH rats. Huperzine A treatment can improve the upregulation of brain water content, damage of blood-brain barrier, fibrinogen and matrix metalloprotein 9 expressions and the downregulation of ZO-1 and occludin expressions induced by SAH. Huperzine A inhibit the expressions of proteins involved in pyroptosis in endothelial cells in SAH rats. The increase in MDA content and decrease in SOD activity in SAH rats can be partly reversed by Huperzine A. The ROS inducer H 2O 2 can induce pyroptosis and inhibit the expressions of ZO-1 and occludin in endothelial cells, which can be blocked by Huperzine A. In addition, the increase in the entry of p65 into the nucleus in endothelial cells can be partly reversed by Huperzine A. Huperzine A may delay the damage of blood-brain barrier in SAH rats by inhibiting oxidative stress-mediated pyroptosis and tight junction protein expression downregulation through the NF-κB pathway. Overall, Huperzine A may have clinical value for treating SAH.

Sex comparison of oxidative stress, mitochondrial dysfunction, and apoptosis triggers induced by single-dose Abamectin in albino rats

Abamectin (AB) is widely used in agriculture and has been employed as an insecticide, nematicide, and livestock pest control agent. However, it may also pose a serious threat to mammals. The primary purpose of this research was to compare the sex variations between male and female rats during exposure and to assess the risk of toxicity of abamectin, which are still largely unknown. The twenty albino rats were divided randomly into four groups (n = 5): 1) the male control group; 2) the male treatment group treated with AB (1 mg/kg B.W.); 3) the female control group; and 4) the female treatment group treated with AB (1 mg/kg B.W.). AB administration caused a drop in body weight in females more than males with showing oxidative stress in both sexes of animals, as characterized by an increase in MDA content and a decrease in glutathione (GSH) content and superoxide dismutase (SOD) activity. Reported sex-specific effects suggested that females are more susceptible from males in brain tissues for alteration of antioxidant markers while females' liver and kidney tissues showed more level of lipid peroxidation than males. In addition, mitochondrial dysfunction was associated with a significant decrease in NADH dehydrogenase (Complex I) and a significant decrease in mitochondrial ATPase, which led to apoptosis and histopathological alterations in the targeted tissues, indicating that females are higher sensitive than males to these biological events. In brief, the results of this study led to female rats are generally more sensitive than male rats to neurobehavioral and hepatic complications associated with abamectin treatment. Further evaluation should be performed to determine the adverse outcome pathways involved and to determine the effects of sex on improving the risk assessment of abamectin in both sexes.

FEATURES FUNCTIONING OF THE DETOXIFICATION SYSTEM AT THE THREAT TERMINATION OF PREGNANCY AS A CONSEQUENCE OF ACCUMULATION OF 137CS

To date, there is no consensus on the pathogenesis of miscarriage. In modern life, human health is signifi cantly infl uenced by environmental factors. In this regard, 37 years after the accident at the Chornobyl nuclear power plant, the question of remote cytogenetic and hereditary eff ects in the off spring of parents aff ected by radiation remains relevant. Ecosystems contaminated with radioactive substances are a source of exposure for humans. Internal irradiation is the cause of reproductive losses. Radiation stress aff ects the course of redox processes in the body. Biochemical indicators are markers of the infl uence of environmental factors on a person. The study is dedicated to determining the state of peroxide hemostasis in the case of miscarriage. Aim: to determine the peculiarities of the functioning of the detoxification system in case of miscarriage due to the accumulation of 137Cs.Material and methods. The fi rst (research) group included women with reproductive losses in anamnesis and signs oftermination of the current pregnancy; the second (control) group included women with an uncomplicated history and course of pregnancy. Additionally, the fi rst group was divided into subgroups according to pregnancy outcomes: А – 38 women who gave birth at 37-40 weeks, despite the complicated course of the current pregnancy, В – 13 women who gave birth at 28-36 weeks + 6 days, С – 9 women who birth at 22-27 weeks + 6 days. The state of peroxide hemostasis in women was studied using biochemical studies. Accumulation of 137Cs with diff erent activity was detected in the placentas of the examined women of both groups using β-spectrometry. Morphological examination of placentas was performed according to the protocol. The severity of placental damage was studied by Olympus BX51 and Axioskop 40 microscopes. Analyzing the results revealed a relationship between biochemical indicators, the activity of 137Cs, and pregnancy scenarios. Statistical data analysis was performed using Microsoft Excel (2016) and Fisher angular transformation. The diff erence between comparative values was considered signifi cant at p &lt; 0.05 (probability index greater than 95 %). Permission to conduct research was obtained from the Medical Ethics Committee of the SI «Institute of Pediatrics, Obstetrics, and Gynecology named academic Elena M. Lukyanova of the National Аcademy of Мedical Sciences of Ukraine» (protocol No 3 of 07.06.2017).Scientifi c research work is to «Develop the latest and improve existing technologies for diagnosis, prevention, and treatmentof premature termination of pregnancy in women with miscarriage taking into account the passport of the placenta» (2018-2020). Code VN.20.00.02.18, state registration number 0118U000039, KPKV 6561040.Results. It has been confi rmed that the state of the environment plays a decisive role in the pathogenesis of miscarriage. Ithas been proven that placental dysfunction caused by abnormal oxidative stress due to the action of incorporated 137Cs leads to pregnancy termination. As a result of the depletion of the antioxidant reserve, the compensatory capabilities of the placenta decrease. It was established that activity in the placenta up to 1.0 Bq/kg of 137Cs does not aff ect the course of gestation. The compensatory capacity of the placenta remains preserved even with the accumulation of 1.1 to 4.4 Bq/kg of 137Cs. At the same time, it is possible to prolong the pregnancy until the term of timely delivery. Internal irradiation with an activity of 4.5-10.4 Bq/kg of 137Cs causes damage to the stroma of the maternal surface of the placenta and premature birth at 28-36 weeks + 6 days. At the same time, newborns are viable due to the preservation of compensatory reactions in the placenta. Accumulation of more than 10.4 Bq/kg of 137Cs causes antenatal death of the fetus and early premature birth due to damage to maternal and fetal structures of the placenta. An increase in the content of malondialdehyde and a decrease in the activity of superoxide dismutase in the blood indicate the severity of radiation damage.Conclusions. Internal exposure to 137Cs disrupts the architecture and functional capacity of the placenta. Extreme eff ectsdepend on the activity of 137Cs, the compensatory capabilities of the placenta, and the pregnant woman’s body. Activation of lipid peroxidation acts as a biochemical amplifi er of radiation exposure. An increase in the blood of malondialdehyde, diene conjugates, and free SH groups is associated with the severity of radiation damage. An early marker of primary placental dysfunction, premature birth, and antenatal fetal loss is an increase in MDA content in the blood by 12.0 % and a decrease in SOD by 6.5 % relative to permissible values. An early marker of exhaustion of the compensatory reserve is an increase in the content of MDA in the blood by 23.3 % and a decrease in SOD by more than 18.2 % relative to the permissible values. Decompensation of adaptation mechanisms in the system «mother- placenta-fetus» leads to antenatal losses.

Growth and physiological responses of submerged macrophytes to linear alkylbenzene sulfonate (LAS)

The potential toxic effects of linear alkylbenzene sulfonate (LAS), widely used in commercial detergents and cleaners, on submerged macrophytes remain unclear. We conducted a two-week exposure experiment to investigate LAS toxicity on five submerged macrophytes (four native and one exotic), focusing on their growth and physiological responses. The results showed that lower concentrations of LAS (< 5 mg/L) slightly stimulated the growth of submerged macrophytes, while higher doses inhibited it. Increasing LAS concentration resulted in decreased chlorophyll content, increased MDA content and POD activity, and initially increased SOD and CAT activities before declining. Moreover, Elodea nuttallii required a higher effective concentration for growth compared to native macrophytes. These findings suggest that different species of submerged macrophytes exhibited specific responses to LAS, with high doses (exceeding 5 ∼ 10 mg/L) inhibited plant growth and physiology. However, LAS may promote the dominance of surfactant-tolerant exotic submerged macrophytes in polluted aquatic environments.

Metal-tolerant morganella morganii isolates can potentially mediate nickel stress tolerance in Arabidopsis by upregulating antioxidative enzyme activities

ABSTRACT Plant growth-promoting rhizobacteria (PGPRs) have been utilized to immobilize heavy metals, limiting their translocation in metal contaminated settings. However, studies on the mechanisms and interactions that elucidate how PGPRs mediate Nickel (Ni) tolerance in plants are rare. Thus, in this study we investigated how two pre-characterized heavy metal tolerant isolates of Morganella morganii (ABT9 and ABT3) improve Ni stress tolerance in Arabidopsis while enhancing its growth and yield. Arabidopsis seedlings were grown for five weeks in control/Ni contaminated (control, 1.5 mM and 2.5 mM) potted soil, in the presence or absence of PGPRs. Plant growth characteristics, quantum yield, and antioxidative enzymatic activities were analyzed to assess the influence of PGPRs on plant physiology. Oxidative stress tolerance was quantified by measuring MDA accumulation in Arabidopsis plants. As expected, Ni stress substantially reduced plant growth (shoot and root fresh weight by 53.25% and 58.77%, dry weight by 49.80% and 57.41% and length by 47.16% and 64.63% over control), chlorophyll content and quantum yield (by 40.21% and 54.37% over control). It also increased MDA content by 84.28% at higher (2.5 mM) Ni concentrations. In contrast, inoculation with M. morganii led to significant improvements in leaf chlorophyll, quantum yield, and Arabidopsis biomass production. The mitigation of adverse effects of Ni stress on biomass observed in M. morganii-inoculated plants was attributed to the enhancement of antioxidative enzyme activities compared to Ni-treated plants. This upregulation of the antioxidative defense mechanism mitigated Ni-induced oxidative stress, leading to improved performance of the photosynthetic machinery, which, in turn, enhanced chlorophyll content and quantum yield. Understanding the underlying mechanisms of these tolerance-inducing processes will help to complete the picture of PGPRs-mediated defense signaling. Thus, it suggests that M. morganii PGPRs candidate can potentially be utilized for plant growth promotion by reducing oxidative stress via upregulating antioxidant defense systems in Ni-contaminated soils and reducing Ni metal uptake.

Dietary Iron Overload Triggers Hepatic Metabolic Disorders and Inflammation in Laying Hen.

Iron, an essential trace element, is involved in various physiological processes; however, consumption of excessive iron possesses detrimental effects. In practical feed production, the iron content added to feeds often far exceeds the actual demand, resulting in an excess of iron in the body. The liver as a central regulator of iron homeostasis is susceptible to damage caused by disorders in iron metabolism. A model of hepatic iron overload in laying hens was developed in this study by incorporating iron into their diet, and the specific mechanisms underlying iron overload-induced hepatic injury were investigated. Firstly, this study revealed that a high-iron diet resulted in hepatic iron overload, accompanied by impaired liver function. Next, assessment of oxidative stress markers indicated a decrease in activities of T-SOD and CAT, coupled with an increase in MDA content, pointing to the iron-overloaded liver oxidative stress. Thirdly, the impact of iron overload on hepatic glycolipid and bile acid metabolism-related gene expressions were explored, including PPAR-α, GLUT2, and CYP7A1, highlighting disruptions in hepatic metabolism. Subsequently, analyses of inflammation-related genes such as iNOS and IL-1β at both protein and mRNA levels demonstrated the presence of inflammation in the liver under conditions of dietary iron overload. Overall, this study provided comprehensive evidence that dietary iron overload contributed to disorders in glycolipid and bile acid metabolism, accompanied by inflammatory responses in laying hens. Further detailing the specific pathways involved and the implications of these findings could offer valuable insights for future research and practical applications in poultry nutrition.

Possible curative effect of venom collected from Algerian bees (Apis mellifera intermissa) on adenine-induced chronic kidney damage in mice

ABSTRACT Chronic kidney disease (CKD) is a world-wide health concern, and thus curative approach becomes highly valuable. Herein, we examined the possible therapeutic effect of bee venom collected from Algeria (Apis mellifera intermissa) on adenine-induced chronic kidney damage. Mice received intraperitoneal injection of adenine at a dose of 50 mg/kg for four weeks to induce CKD. After that, bee venom was administered intraperitoneally (i.p) to mice at a dose of 0.76 mg/kg BW for a week. Adenine-treated mice decreased the body weight evolution, and significantly increased the kidney weight, water intake, and urine output compared with controls. In addition, serum and urine urea and creatinine levels, and serum albumin concentrations were significantly increased, while serum creatinine clearance level was significantly decreased in adenine-treated mice compared with controls. Adenine-induced oxidative stress was evidenced by increased MDA content, and decreased catalase and GST activity, and GSH content in renal tissue. Meanwhile, the administration of bee venom to adenine-treated mice markedly recovered kidney function via improvement of the altered physiological and biochemical parameters. These were confirmed by the morphological and histopathological results. In conclusion, bee venom is a prising therapeutic natural agent for improving kidney function in adenine-induced CKD.

RNA-Seq analysis reveals the mechanism in response to cold stress of peach cv ‘Dingjiaba’

BACKGROUND: ‘Dingjiaba’ is an important Prunus persica cultivar (cv) mainly grown in the Hexi corridor in northwest China, which has an inherited strong cold tolerance. OBJECTIVE: To compare the transcriptome and physiology data of leaves of cvs ‘Dingjiaba’ (D) and ‘Kanoiwa’ (K) following cold treatment at different time periods, in order to gain new insights into the mechanisms of cold adaptation in ‘Dingjiaba’. MATERIALS AND METHODS: We analyzed the transcriptomic and physiological data of leaves of D and K cvs exposed to 0 h (D0/K0), 2 h (D2/K2), 6 h (D6/K6) and 12h (D12/K12) cold stress. RESULTS: Low temperature stress caused membrane damage and led to increased rate of electrolyte leakage and increased MDA content. Cold stress induced the accumulation of soluble sugars, soluble proteins and proline in leaves of both cvs, with a lower increase in K compared to D. Transcriptome analysis identified 4,631, 5,069, 5,662 and 3,886 differentially expressed genes (DEGs) between D0 and K0, D2 and K2, D6 and K6 and D12 and K12, respectively. The differentially expressed genes significantly enriched in metabolic pathways and biosynthesis of secondary metabolites. We further validated the reliability of sequencing data of the RNA-Seq with Real-Time Quantitative PCR, which suggested that the expression trend of the RNASeq were same as RT-PCR. CONCLUSIONS: These results provide novel insights into a series of molecular mechanisms underlying physiological metabolism and defense.