Glutathione S-transferase Activity Research Articles

Selective Lipophilization of Natural Phenolic Alcohols Induced by In Situ Choline Chloride-Based Natural Deep Eutectic Solvents.

In this scientific work, a novel and green method for selective lipophilization of EVOO's bioactive phenolic alcohols (PAs), namely, tyrosol, hydroxytyrosol, and its metabolite homovanillyl alcohol as fatty acid esters, is elucidated. The PAs have been employed as hydrogen bond donors in the formation of natural deep eutectic solvents (NADES) with choline chloride (ChCl). The fast and cheap esterification method by in situ formation of choline chloride-based deep eutectic solvents promotes the derivatization of PAs with various fatty acids as acylating agents in the absence of organic solvents and catalysts. Furthermore, given the growing interest in the application of NADES formed by bioactive molecules in the pharmacological and cosmetic fields, we analyzed the activity of antioxidant enzymes, superoxide dismutase, and glutathione S-transferase of three chemical formulations obtained after the formation of PA-oleate in the H2O2-treated HaCat human keratinocytes cell line, assessing also their toxicity via the MTT assay.

DEHP impairs the oxidative stress response and disrupts trace element and mineral metabolism within the mitochondria of detoxification organs.

Di(2-ethylhexyl) phthalate (DEHP), a widely utilized plasticizer in various consumer products, is classified as an endocrine disruptor and has been implicated in numerous adverse health effects, including oxidative stress, inflammation, and metabolic disturbances. Despite the growing body of literature addressing the systemic effects of DEHP, the specific influence of DEHP-induced oxidative stress on mitochondrial function within detoxification organs, particularly the liver and kidneys, remains largely unexplored. This study evaluated the effects of DEHP exposure (0, 100, 200, and 400mg/kg/day) on mitochondrial oxidative stress, trace elements, and mineral metabolism associated with signaling pathways in the liver and kidneys of rats. Altered mitochondrial oxidative stress status was indicated by impaired glucose 6-phosphate dehydrogenase (G6PD), 6-phosphoglucerate dehydrogenase (6-PGD), glutathione reductase (GR), glutathione s-transferase (GST), and glutathione peroxidase (GPx) activities, along with significant disruptions in essential minerals and trace elements, including Na, Mg, Cu, Zn, and Fe. Key oxidative stress signaling pathways, such as NF-κB, Akt, STAT3, and CREB, glucose, and tissue homeostasis, displayed dose-dependent responses to DEHP, indicating complex regulatory mechanisms. This study represents the first comprehensive investigation into DEHP-induced mitochondrial dysfunction, highlighting its effects on oxidative stress metabolism, trace element homeostasis, and cellular signaling pathways in detoxification organs. These findings provide novel insights into the mitochondrial mechanisms underlying DEHP toxicity and underscores the need for further research into the implications of plasticizer exposure on human health.

Mondia whitei fruit extract abates cadmium chloride-induced nephrotoxicity via the suppression of oxidative stress in rats

Cadmium (Cd) is an industrial heavy metal that causes toxic effects to several body organs including the kidney. Medicinal plants are used in managing various diseases caused by environmental toxicants. This study aimed to evaluate the protective ability of Mondia whitei fruit extract (MWE) against nephrotoxicity induced by CdCl₂ exposure in Wistar rats. Twenty-five male Wistar rats of 90 to 130 g body weight (b.w) were used in this study. The animals were indiscriminately assigned to five groups of five animals per group. The control group were rats in group I, whereas group II to V rats were orally administered CdCl₂ (5 mg/kg body weight (b.w)) for 5 days. Simultaneously, the rats in group III to V were co-treated with 70 mg/kg b.w of silymarin, 250 and 500 mg/kg b.w of MWE, respectively. The CdCl2 significantly (p < 0.05) increased the levels of serum renal biomarkers such as urea and creatinine, total protein and albumin. Furthermore, a substantial (p < 0.05) elevation in the nitric oxide (NO) and malondialdehyde (MDA) levels, and a concomitant (p < 0.05) reduction in the kidney activities of superoxide dismutase (SOD) and glutathione transferase (GST), and the level of reduced glutathione (GSH) were observed in the CdCl2-intoxicated rats. Alterations in the kidney's histology were also noted. Nonetheless, treatment with MWE markedly returned to normal the levels of serum kidney parameters and tissue NO and MDA. In addition, the MWE significantly (p < 0.05) elevated tissue antioxidant levels and restored the kidney histology. The result of this study suggest that MWE could potentially serve as an alternative therapy in managing CdCl2-induced nephrotoxicity.

Glutathione S-Transferase Contributes to the Resistance of Megalurothrips usitatus Against Lambda-Cyhalothrin by Strengthening Its Antioxidant Defense Mechanisms.

The damage caused by Megalurothrips usitatus, a common pest, has significantly affected the Chinese vegetable industry. The inappropriate application of chemical pesticides has caused M. usitatus to become highly resistant to conventional insecticides. Glutathione S-transferase (GST), known for its multifunctional properties, contributes to detoxification and antioxidation. It enhances insects' adaptability to pesticides by facilitating the elimination of lipid peroxidation products resulting from pyrethroid insecticides. This research employed RT-qPCR to identify GST genes that exhibited significant expression in response to lambda-cyhalothrin stress. It also quantified changes in antioxidant and apoptosis markers within the M. usitatus under lambda-cyhalothrin exposure. The functional significance of GST was validated by assessing alterations in the antioxidant defense system and resistance to lambda-cyhalothrin following the inhibition of GST activity. The study's outcomes indicated that MuGSTs1 was markedly upregulated in response to lambda-cyhalothrin stress (p < 0.0001). The GST activity was effectively suppressed by the specific inhibitor, diethyl maleate, achieving an inhibition rate of 64.05%. Following the inhibition of GST, the overall antioxidant capacity was reduced by 3.1-fold compared with the control, and the M. usitatus exhibited a 7.91-fold increase in sensitivity to lambda-cyhalothrin. These findings confirm the pivotal role of GST in the oxidative stress response of the M. usitatus and their contribution to the development of resistance to lambda-cyhalothrin through enhanced antioxidant defenses. This research offers valuable perspectives on the adaptive reactions of insects to chemical stressors, facilitating the management of resistance and the formulation of effective pest control strategies.

The combined effect of environmentally relevant doses of glyphosate and high temperature: An integrated and multibiomarker approach to delineate redox status and behavior in Danio rerio.

Glyphosate, a pesticide commonly found in aquatic ecosystems, affects this habitat and nontarget organisms such as fish. The increase in water temperature, linked to factors such as climate change, poses a considerable threat. Despite extensive ecotoxicological research, we still do not know the real individual and specific consequences of continued exposure to glyphosate and high temperatures, simulating a scenario where the aquatic environment remains contaminated and temperatures continue to rise. Therefore, in this study, we examined the effects of exposure to environmentally relevant concentrations of glyphosate, active ingredient glyphosate (GAI), and glyphosate-based herbicide (GBH) in combination with high temperature (34 °C) in adult zebrafish (Danio rerio). The fish were acclimated to 28 or 34 °C for 96 h. The exposure to 225 and 450 μg L-1 (GBH or GAI) at 28 or 34 °C for 7 days. We analyzed behavioral endpoints (anxiety-like response, sociability, and aggressivity) and biochemical biomarkers of the brain and muscle (oxidative stress). Anxiety-like responses and decreased sociability were disrupted by the combination of glyphosate and high temperature. Furthermore, there is a decrease in Acetylcholinesterase activity in the brain, and an increase in Lipid Peroxidation, Protein Carbonylation, Acetylcholinesterase activity, and Glutathione S-Transferase activity in the muscle. These results demonstrated oxidative stress, anxiety-like behavior and decreased sociability caused by glyphosate and high temperature. We concluded that the combined effects of glyphosate and high temperature affected redox homeostasis and behavior, emphasizing that the field of glyphosate pollution should be carefully considered when evaluating the effects of climate change.

Species-specific responses to di (2-ethylhexyl) phthalate reveal activation of defense signaling pathways in California sea lion but not in human skeletal muscle cells in primary culture.

Higher antioxidant defenses in marine than terrestrial mammals allow them to cope with oxidative stress associated with diving-induced ischemia/reperfusion. Does this adaptation translate to inherent resistance to other stressors? We analyzed oxidative stress indicators in cells derived from human and California sea lion (Zalophus californianus) skeletal muscle upon exposure to di (2-ethylhexyl) phthalate (DEHP). Human abdominal muscle biopsies were collected from healthy women undergoing planned cesarean surgery. California sea lion samples were collected postmortem from stranded animals. Skeletal muscle cells derived from each species were exposed to 1 mM DEHP for 13 days (n = 25) or maintained under control (untreated) conditions (n = 25). Superoxide radical (O2-) production, oxidative damage and antioxidant enzyme activities were measured using spectrophotometric methods. Gene expression was analyzed by RT-qPCR. DEHP exposure increased O2- production and superoxide dismutase (SOD) activity in both species. Glutathione S-transferase (GST) activity and protein carbonyls levels increased in human but not in California sea lion cells. In contrast, glutathione peroxidase (GPx) and catalase (CAT) activities increased in California sea lion but not in human cells exposed to DEHP. In human cells, DEHP increased microsomal GST1 and GST (κ, μ, θ, ω, and ᴢ), while suppressing 8-oxoguanine DNA glycosylase (OGG1), CAT, glutathione reductase (GR), and nuclear factor erythroid 2-related factor 2 (NRF2) expression, suggesting increased oxidative stress and phase two detoxification processes. In California sea lion cells, DEHP increased OGG1, NRF2, GPx2 and SOD3 expression, suggesting activation of antioxidant defenses, which potentially contribute to maintaining redox homeostasis, avoiding oxidative damage.

Female rat liver after sub-acute dibutyl phthalate treatment: Histological, stereological, biochemical, and global gene expression study

Although it has been recognized that females are more susceptible to chemical-induced liver injury, the effects of dibutyl phthalate (DBP), a widely used synthetic chemical, on female liver structure and function are under-researched. Here, we sought to investigate the effects of DBP on histological, stereological, and biochemical parameters, as well as global gene expression in female rat liver. Female Wistar rats were exposed to 100, 500, and 5000 mg DBP/kg diet for 28 days, corresponding to 8.6, 41.43, and 447.33 mg DBP/kg body weight (B.W.)/day, respectively. The highest dose (447.33 mg DBP/kg B.W./day) was between the no-observed-adverse-effect level (NOAEL) and the lowest-observed-adverse-effect level for liver toxicity, whereas two lower doses (8.6 and 41.43 mg DBP/kg B.W./day) were below the NOAEL. Analysis of hematoxylin and eosin-stained sections revealed an increased volume of hepatocytes, their nuclei and cytoplasm, while the volume of sinusoids decreased in DBP-exposed groups compared to the control. Examination of Periodic acid-Schiff-stained sections showed reduced glycogen content, which was the most prominent in the highest dose group. Increased glutathione S-transferase and catalase activities, and decreased GSH content and superoxide dismutase activity were observed in DBP-exposed groups. The mRNA sequencing revealed DBP-induced dose-specific changes in various genes and biological functions in female rat liver. The highest number of deregulated genes was observed in the 500 mg DBP/kg diet group. In summary, exposure to DBP caused significant liver microstructural changes, decreased glycogen content, disturbed the redox status, and affected global gene expression in female rat liver.

SIRT2-mediated deacetylation of glutathione transferase alleviates oxidative damage and increases the heat tolerance of Pleurotus ostreatus

High-temperature stress (HS) severely threatens agricultural production. Pleurotus ostreatus is cultivated in many parts of the world, and its growth is strongly affected by HS. We previously reported that metabolic rearrangement occurred in HS, but the gene expression levels of several key enzymes remained unchanged. Therefore, in this study, we investigated the contribution of posttranslational modifications of proteins to HS resistance in P. ostreatus. We found that the level of acetylation of P. ostreatus decreased under short-term HS treatment and increased as the duration of HS treatment increased. Acetylation omics revealed that almost all metabolic enzymes were acetylated. We found that deacetylation under HS can improve the growth recovery ability of mycelia, the activity of matrix-degrading enzyme, and the contents of antioxidants, such as nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), but can decreased H2O2 levels. In vitro acetylation experiments and point mutations revealed that the deacetylase SIRT2 increased the activity of glutathione transferases (GSTs) by deacetylating GST1 66K, GST2 206K, and GST2 233K. Together, SIRT2 is activated by short-term HS and improves its antioxidant activity by deacetylating GSTs, thereby improving the resistance of P. ostreatus to HS. In this study, we identified new non-histone substrate proteins and new lysine acetylation sites of SIRT2 under HS. We also discovered the role of non-histone acetylation in the adaptation of organisms to HS.

Glutathione S-transferase: A keystone in Parkinson's disease pathogenesis and therapy.

Parkinson's disease is a progressive neurodegenerative disorder that predominantly affects motor function due to the loss of dopaminergic neurons in the substantia nigra. It presents significant challenges, impacting millions worldwide with symptoms such as tremors, rigidity, bradykinesia, and postural instability, leading to decreased quality of life and increased morbidity. The pathogenesis of Parkinson's disease is multifaceted, involving complex interactions between genetic susceptibility, environmental factors, and aging, with oxidative stress playing a central role in neuronal degeneration. Glutathione S-Transferase enzymes are critical in the cellular defense mechanism against oxidative stress, catalysing the conjugation of the antioxidant glutathione to various toxic compounds, thereby facilitating their detoxification. Recent research underscores the importance of Glutathione S-Transferase in the pathophysiology of Parkinson's disease, revealing that genetic polymorphisms in Glutathione S-Transferase genes influence the risk and progression of the disease. These genetic variations can affect the enzymatic activity of Glutathione S-Transferase, thereby modulating an individual's capacity to detoxify reactive oxygen species and xenobiotics, which are implicated in Parkinson's disease neuropathological processes. Moreover, biochemical studies have elucidated the role of Glutathione S-Transferase in not only maintaining cellular redox balance but also in modulating various cellular signalling pathways, highlighting its neuroprotective potential. From a therapeutic perspective, targeting Glutathione S-Transferase pathways offers promising avenues for the development of novel treatments aimed at enhancing neuroprotection and mitigating disease progression. This review explores the evident and hypothesized roles of Glutathione S-Transferase in Parkinson's disease, providing a comprehensive overview of its importance and potential as a target for therapeutic intervention.

Effects of copper nanoparticles synthesized from the entomopathogen Metarhizium robertsii against the dengue vector Aedes albopictus (Skuse, 1894).

Aedes albopictus, known as the Asian tiger mosquito, is a significant vector for dengue fever, chikungunya, zika virus, yellow fever. Current control methods rely on chemical insecticides, which face challenges such as resistance, environmental harm, and impact on non-target species Eudrilus eugeniae and Artemia salina. This study evaluates the toxic effects of biogenic copper nanoparticles (CuNPs) synthesized using Metarhizium robertsii intracellular extract obtained from our previous research. The CuNPs were tested against A. albopictus and non-target species at 24 and 48 hours post-treatment. Results demonstrated that entomopathogenic fungi-derived CuNPs exhibited potent mosquitocidal activity, resulting in 97.33% mortality in larvae, 93.33% in pupae, and 74.66% in adults at 48 hours post-treatment. The CuNPs derived from M. robertsii showed lower LC50 values of 74.873 mg/L in larvae, 76.101 mg/L in pupae, and 136.645 mg/L in adults at 48 hours post-treatment. Additionally, 12 hours post-treatment, catalase (an antioxidant enzyme) activity decreased 1.5-fold in a dose-dependent manner, while glutathione S-transferase (a detoxification enzyme) activity increased 7.8-fold. CuNPs demonstrated lower toxicity to non-target species, with 24% mortality in A. salina and 24.44% mortality in E. eugeniae at 24 hours post-treatment. The LC50 values were 634.747 mg/L for A. salina and 602.494 mg/L for E. eugeniae at 24 hours post-treatment. These findings indicate that entomopathogenic fungi-derived CuNPs are a promising, target-specific candidate for controlling A. albopictus at various life stages (larvae, pupae, and adults).

Glyphosate and glyphosate-based herbicides induce Poecilia reticulata to maintain redox equilibrium during and after coexposure to iron oxide nanoparticles (y-Fe2O3)

Iron oxide nanoparticles (IONPs) are being increasingly recognized as viable materials for environmental remediation due to their capacity to adsorb contaminants such as glyphosate (GLY) on their surfaces. Nevertheless, the ecotoxicological implications of IONPs associated with GLY necessitate thorough evaluation to ascertain the safety of such remediation strategies. In this context, the present investigation was conducted to examine hepatic biomarkers pertinent to the redox system, as well as ultrastructural hepatic alterations in Poecilia reticulata, following a 21-day exposure to environmentally relevant concentrations of IONPs, iron ions (Fe), and glyphosate in its pure form (GLY) as well as a commercial glyphosate-based herbicide (GBH). After this exposure, the fish underwent a 21-day recovery in uncontaminated water. The results indicated an increase in the activity of catalase (CAT) and glutathione S-transferase (GST) and in the concentration of glutathione (GSH) in the animals subjected to IONP+GBH and IONP+GLY treatments. This biochemical response persisted for the duration of both the exposure and recovery phases. Concurrently, hepatocytes displayed mitochondria with increased electron density, augmented lipid droplet accumulation, and expanded necrotic areas within the hepatic tissue. In contrast, fish exposed solely to IONPs exhibited sustained redox homeostasis throughout the investigative timeline. These findings suggest that the coexposure toxicity of IONP+GLY and IONP+GBH is attributable to the agent adsorbed onto the IONPs and that P. reticulata could maintain an active antioxidant defense mechanism throughout the entire study period.

Nanoformulation of imidacloprid insecticide with biocompatible materials and its ecological and physiological effects on wheat green aphid, Schizaphis graminum Rondani

Nanoformulation of imidacloprid was prepared using the biocompatible polymer of polyethylene glycol (PEG). TEM image showed that the spherical nanoparticles were 50–150 nm. The lethal concntrationof 30 percent (LC30) and 50 percent (LC50) of the insecticide and its nanoformulation studied on adult female aphids were 21.46 and 58.56 mg a.i./L for pure insecticide, and 3.79 and 4.94 mg a.i./L for nanoformulated insecticide, respectively. The results of the sublethal effect test (LC30) of this insecticide showed that nymphal developmental in nanoimidacloprid (5.55 days) was higher than control (4.22 days). The results showed that the insecticide treatments significantly reduced the demographic characteristics of Schizaphis graminum. The intrinsic rates of increase (r) values of aphids in control, insecticide treatment and its nanoformulation were 0.421, 0.315 and 0.29, respectively. The results of evaluating the effect of the studied insecticide on the specific activity of beta-esterase and glutathione S-transferase showed that there was no significant difference in the activity of this enzymes between the control and the insecticide treatment and its nanoformulation. Based on the obtained results, it can be concluded that after conducting additional tests, the insecticide nanoformulation can be used due to its effectiveness in lower concentrations in the management of sucking pests such as aphids.

Biochemical and proteomic approaches to investigating effects of IAA-aspartate in pea (Pisum sativum L.) seedlings during osmotic shock

Osmotic shock is the first step of high salt or drought action that involves biochemical and molecular changes during plant response to these unfavorable conditions. Indole-3-acetyl-aspartate (IAA-aspartate, IAA-Asp) is the main amide conjugate of auxin in pea (Pisum sativum L.) tissues. Although the exact molecular mechanism of the IAA-Asp action is unknown, this conjugate's indole-3-acetic acid (IAA)-independent biological activity has been observed during physiological and stress conditions. In this work, we investigated the effect of IAA-Asp alone, as well as in combination with NaCl or polyethylene glycol (PEG) (osmotic shock) on reduced/oxidized glutathione (GSH/GSSG) ratio, activities of enzymes modulating glutathione concentration, protein S-glutathionylation, and IAA homeostasis. We did not observe the hydrolysis of IAA-Asp to IAA in pea seedlings, which, together with other results, suggests that IAA-Asp modulates plant response to abiotic stimuli independently of IAA. Moreover, despite the effect of IAA-Asp on the enzymes responsible for IAA conjugation, no changes in this phytohormone level were visible. Furthermore, 3h plant treatment with IAA-Asp increased the activity of glutathione reductase (GR), which correlates with an elevated GSH/GSSG ratio. On the contrary, more extended (48h) incubation with IAA-Asp diminished the GSH/GSSG ratio and increased the activity of glutathione peroxidase (GPX). IAA-Asp reduced GR activity during salt treatment but did not affect the GSH/GSSG ratio. Similarly, under plant incubation with PEG, IAA-Asp did not change the GSH/GSSG ratio but increased glutathione S-transferase (GST) activity. We also analyzed the effect of IAA-Asp on pea protein S-glutathionylation. Increased S-glutathionylation of heat shock 70 kDa protein (HSP70) was observed after plant treatment with IAA-Asp, PEG, or IAA-Asp combined with PEG. The proteomic analysis also revealed that IAA-Asp diminished S-glutathionylation of lipoxygenase during plant incubation with PEG. Thus, we suggest that IAA-Asp modulates redox status in pea during oxidative stress and under normal physiological conditions.

Garlic Bulb Essential Oil (GBEO) as a Potential Mitigator of Lead Nitrate-Induced Oxidative Stress in Swiss Albino Male Mice

This research examined the effectiveness of essential oil derived from garlic bulb in alleviating the toxic effects of lead nitrate in animal model Swiss albino mice. Six groups were considered for the study, Group I was untreated and Group II to Group VI animals were given lead nitrate at the dose of 50 mg/kg orally for 30 days. Group III and Group IV received low dose (50 mg/kg), high dose (80 mg/kg) of GBEO, and Group V was given standard drug (Silymarin) respectively, lastly Group VI was given olive oil to see its effect alone, from the 12th day until the experiment’s conclusion. To assess GBEO protective effects, various antioxidant parameters, including Superoxide Dismutase (SOD) activity, Lipid Peroxidation (LPO) activity, Glutathione (GSH) levels, Activity of Glutathione Peroxidase (GPx), Catalase (CAT) activity, and levels of Glutathione S-Transferase (GST) were evaluated in Swiss albino mice testicular homogenate. The results revealed that GBEO, particularly the high dose, significantly mitigated lead-induced oxidative stress. This was evidenced by improvements in antioxidant enzyme potencies and preserved GSH levels. These findings indicate that GBEO holds a promising prophylactic treatment for lead poisoning. However, further studies are warranted to optimize the dosing regimen for maximizing its protective efficacy against lead toxicity.

Carvacrol modulates antioxidant enzymes, DNA integrity, and apoptotic markers in zearalenone-exposed fetal rat liver

Maternal exposure to zearalenone (ZEA), a mycotoxin, can impact fetal liver development. This study investigated the protective effects of carvacrol (CRV) against ZEA-induced fetal liver damage. Thirty-two pregnant rats were allocated to four groups (eight rats/group); control, CRV (75 mg/kg), ZEA (5 mg/kg), and co-treated group (ZEA + CRV). The animals were given their doses during the gestation period. Maternal exposure to ZEA revealed a significant increase in the malondialdehyde (MDA) level in the fetal liver. In contrast, glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities, besides glutathione (GSH) levels, were decreased in ZEA-intoxicated rats. Additionally, ZEA increased the expression of pro-apoptotic genes (P53, Bax, and caspase-9), elevated the immunoreactivity of caspase-3, decreased anti-apoptotic Bcl-2, and induced severe fatty degeneration, congestion, and necrosis in the fetal liver. The comet assays revealed significant DNA damage, as evidenced by reduced head DNA content and increased tail DNA content and tail moment in the ZEA-exposed rats. Surprisingly, co-treatment with CRV significantly mitigated fetal hepatic lipid peroxidation, antioxidant disturbance, apoptosis, and DNA damage after maternal exposure to ZEA. These findings highlight the potential of CRV as a promising approach to mitigate ZEA-associated developmental hepatotoxicity.

Bioorthogonal Chemistry-Guided Inhalable Nanoprodrug to Circumvent Cisplatin Resistance in Orthotopic Nonsmall Cell Lung Cancer.

Pulmonary delivery of anticancer therapeutics has shown encouraging performance in treating nonsmall cell lung cancer (NSCLC), which is characterized by high aggressiveness and poor prognosis. Cisplatin, a key member of the family of DNA alkylating agents, is extensively employed during NSCLC therapy. However, the development of chemoresistance and the occurrence of side effects severely impede the long-term application of cisplatin-based chemotherapies. Herein, we propose a meaningful strategy to precisely treat cisplatin-resistant NSCLC based on the combination of bioorthogonal chemistry with an inhalation approach. Ethacraplatin (EA-Pt), a platinum prodrug (IV), was synthesized and encapsulated in nitric oxide (NO)-containing micelles to overcome cisplatin chemoresistance. By further modifying bioorthogonal molecules in this nanoplatform (EA-Pt@MDBCO), an improved targeting performance toward pulmonary cancerous regions is achieved after prelabeling with azide via inhalation. Upon entering acidic cancer cells, EA-Pt is swiftly released due to the pH sensitivity of bioorthogonal micelles, which enables its bifunctions to inhibit glutathione S-transferase activity and deplete intracellular glutathione, eventually reversing cisplatin resistance. Moreover, the released NO also improves the overall therapeutic outcome against NSCLC. Consequently, inhalable EA-Pt@MDBCO prelabeled by azide effectively inhibits the progression of cisplatin-resistant orthotopic NSCLC, offering a feasible nanostrategy to expand the treatment options for NSCLC.

Comparative analysis of active period and oxidative stress of DDVP and ginger (Zingiber officinale) oil on Indian meal moth (Plodia interpunctella Hübner) infesting maize grain

BackgroundIndian meal moth (Plodia interpunctella) is a significant pest infesting stored grains, particularly maize. Over time, synthetic insecticides have been employed to control insect. The residual effects posed on non-target organisms have called for replacement of synthetic insecticides with botanicals. This study therefore aimed at comparing the insecticidal consistency and oxidative stress invoked by dichlorvos (DDVP) and the oil extract of ginger (Zingiber officinale) on Indian meal moth infesting maize. Disinfested maize grains were treated with DDVP and ginger oil extract separately. Adults P. interpunctella were introduced to the treated grains daily using complete replacement method. The percentage mortality was calculated daily for 10 d. Furthermore, the oxidative stress caused by DDVP and ginger oil extract on the moth was evaluated by measuring the level of some oxidative stress biomarkers such as glutathione S-transferase, superoxide dismutase, glutathione peroxidase (GPx), and catalase (CAT) activity in the exposed insects.ResultsPreliminary results indicated that both DDVP and ginger oil extract exhibited insecticidal properties against Indian meal moth infesting maize. However, the insecticidal (active) period of ginger oil extract was found to be longer than that of DDVP. Nevertheless, DDVP provoked greater oxidative stress in the exposed moth.ConclusionsGinger oil extract and DDVP show potential for controlling Indian meal moth infestations in stored maize. Yet, ginger oil offers a longer-lasting effect on pest suppression and control. Consequently, it could be a replacement or synergistic insecticide with DDVP to provide ecofriendly insecticide application.

The Impact of Perfluorooctanoic Acid (PFOA) on the Mussel Mytilus galloprovincialis: A Multi-Biomarker Evaluation

Perfluorooctanoic acid (PFOA) has been widely studied due to its environmental persistence and bioaccumulation potential, raising concerns about its effects on aquatic life. This research evaluates the impact of PFOA on the antioxidant defenses and stress response systems of the mussel Mytilus galloprovincialis. Mussels were exposed to three concentrations of PFOA (1, 10, and 100 µg·L−1) over 28 days. Several biomarkers, including glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO), total antioxidant capacity (TAC), vitellogenin (VTG), ubiquitin (UBI), and caspase-3 (CASP) were analyzed. The results suggest stress responses, particularly in animals exposed to higher concentrations, as shown by GST and SOD activities which increased according to PFOA concentrations. Additionally, oxidative stress markers such as MDA and CAT showed variable responses depending on the exposure concentration tested. This study underscores the need for further investigation into the effects of PFOA on mollusks but also the need to unveil gender-specific responses in aquatic organisms exposed to this contaminant. The concentrations of PFOA used in our research are lower than those examined in previous studies, providing crucial insights into the impacts of even minimal exposure levels. It highlights the potential of M. galloprovincialis as a bioindicator in environmental monitoring programs, providing crucial insights for environmental management and policymaking regarding regulating and monitoring PFOA in marine settings. Consequently, in a country where seafood consumption is the second largest in Europe, implementing environmental policies and regulatory measures to manage and monitor PFOA levels in marine environments is crucial.

Inter- and intraspecific blood-related biomarkers and chemical exposure in confined and free-living sea turtles.

The relevance of recovery centers and head-starting programs for rescue, rehabilitation, rearing, and conservation of sea turtles is recognized worldwide. In addition, these centers contribute to generating biochemical and physiological data needed to identify health markers and provide baseline values. Because of the marine ecosystems' deterioration, biomarker identification is a global priority for sea turtle conservation; nevertheless, information on specific endpoints, such as neurotoxicity and mutagenesis, is still limited in sea turtles. This study aimed to contrast a set of non-invasive blood biomarkers with ecotoxicological and clinical applications in confined green sea turtles (Chelonia mydas) compared with free-living ones from the Mexican Caribbean. Additionally, interspecific (green, hawksbill (Eretmochelys imbricata), loggerhead (Caretta caretta) turtles) differences were also evaluated. Plasmatic organochlorine pesticides (OCs) and polychlorinated biphenyl (PCBs) were also determined. The concentration ranges of uric acid, total proteins, lipids (cholesterol and triglycerides), and thyroxine of both confined and free-living green turtles fell outside the reference intervals for the species. Additionally, confined green turtles had the highest number of erythrocytic nuclear abnormalities (ENA) and elevated levels of hemoglobin, lipid peroxidation, and activity of glutathione S-transferase, glutathione peroxidase, and carboxylesterase (CE). Contrasts among confined species identified hawksbill turtles with the lowest glutathione reductase activity, green turtles with the lowest ENA frequency and CE activity, and loggerhead turtles with the highest plasmatic concentrations of PCBs and OCs. The information here provided can be used as information in health monitoring programs and for conservation and management policies at regional, national, and international level.

Short-term exposure to okadaic acid induces behavioral and physiological responses in sea urchin (Strongylocentrotus intermedius)

Massive harmful algal blooms (HABs) have increased the risk of marine organisms encountering the dinoflagellate toxin, okadaic acid (OA). Strongylocentrotus intermedius, a globally significant benthic aquaculture species, has a large appetite for benthic algae. During red tide events, there is a high risk of red tide toxin accumulation. This study systematically evaluated the potential impact of short-term OA exposure on the behavior and physiological functions of juvenile S. intermedius. From typical (5 μg/L) to extreme OA concentrations (20 μg/L) during HAB outbreaks, OA exposure gradually inhibited a series of tube foot-related behaviors (sheltering, foraging, righting, and tube-foot tenacity). At OA concentrations during HAB outbreaks (5 μg/L), the tube foot function of S. intermedius was progressively inhibited. Further physiological indicator analyses revealed that the activity of antioxidants increased over a short period to prevent damage from reactive oxygen species induced by OA. However, OA ultimately suppressed the immune response of S. intermedius, leading to apoptosis. Although HAB-associated concentrations of OA (5 μg/L) did not induce a continuous increase in the integrated biological response index of S. intermedius, this study speculated that HABs pose a future risk to echinoderm species. Notably, principal component analysis results showed that OA exposure eventually induced significant changes in the production of O2-, malondialdehyde, and total glutathione, as well as in glutathione S-transferase activity and caspase-7, -8, and -9 levels. This study provides preliminary evidence of OA’s toxic effects on sea urchins and essential data for urgent risk assessments of algal toxin pollution in aquaculture during HABs.