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1.
Biomed Pharmacother ; 177: 117117, 2024 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-38996709

RESUMEN

The incidence of diabetes is increasing annually, and the disease is uncurable due to its complex pathogenesis. Therefore, understanding diabetes pathogenesis and developing new treatments are crucial. This study showed that the NO donor SNP (8 µM) significantly alleviated high glucose-induced developmental toxicity in zebrafish larvae. High glucose levels caused hyperglycemia, leading to oxidative stress and mitochondrial damage from excessive ROS accumulation. This promoted mitochondrial-dependent apoptosis and lipid peroxidation (LPO)-induced ferroptosis, along with immune inflammatory reactions that decreased mitochondrial function and altered intracellular grid morphology, causing imbalanced kinetics and autophagy. After SNP treatment, zebrafish larvae showed improved developmental toxicity and glucose utilization, reduced ROS accumulation, and increased antioxidant activity. The NO-sGC-cGMP signaling pathway, inhibited by high glucose, was significantly activated by SNP, improving mitochondrial homeostasis, increasing mitochondrial count, and enhancing mitochondrial function. It's worth noting that apoptosis, ferroptosis and immune inflammation were effectively alleviated. In summary, SNP improved high glucose-induced developmental toxicity by activating the NO-sGC-cGMP signaling pathway to reduce toxic effects such as apoptosis, ferroptosis and inflammation resulting from mitochondrial homeostasis imbalance.


Asunto(s)
Homeostasis , Larva , Mitocondrias , Pez Cebra , Animales , Mitocondrias/metabolismo , Mitocondrias/efectos de los fármacos , Mitocondrias/patología , Homeostasis/efectos de los fármacos , Larva/efectos de los fármacos , Apoptosis/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal/efectos de los fármacos , Glucosa/metabolismo , Glucosa/toxicidad , Óxido Nítrico/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Ferroptosis/efectos de los fármacos
2.
Toxics ; 12(7)2024 Jun 29.
Artículo en Inglés | MEDLINE | ID: mdl-39058127

RESUMEN

Micro- and nano-plastics (MNPs) are ubiquitously distributed in the environment, infiltrate organisms through multiple pathways, and accumulate, thus posing potential threats to human health. MNP exposure elicits changes in microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), thereby precipitating immune, neurological, and other toxic effects. The investigation of MNP exposure and its effect on miRNA expression has garnered increasing attention. Following MNP exposure, circRNAs serve as miRNA sponges by modulating gene expression, while lncRNAs function as competing endogenous RNAs (ceRNAs) by fine-tuning target gene expression and consequently impacting protein translation and physiological processes in cells. Dysregulated miRNA expression mediates mitochondrial dysfunction, inflammation, and oxidative stress, thereby increasing the risk of neurodegenerative diseases, cardiovascular diseases, and cancer. This tract, blood, urine, feces, placenta, and review delves into the biotoxicity arising from dysregulated miRNA expression due to MNP exposure and addresses the challenges encountered in this field. This study provides novel insights into the connections between MNPs and disease risk.

3.
Toxics ; 12(7)2024 Jul 05.
Artículo en Inglés | MEDLINE | ID: mdl-39058145

RESUMEN

Due to their robust migration capabilities, slow degradation, and propensity for adsorbing environmental pollutants, micro(nano)plastics (MNPs) are pervasive across diverse ecosystems. They infiltrate various organisms within different food chains through multiple pathways including inhalation and dermal contact, and pose a significant environmental challenge in the 21st century. Research indicates that MNPs pose health threats to a broad range of organisms, including humans. Currently, extensive detection data and studies using experimental animals and in vitro cell culture indicate that MNPs can trigger various forms of programmed cell death (PCD) and can induce various diseases. This review provides a comprehensive and systematic analysis of different MNP-induced PCD processes, including pyroptosis, ferroptosis, autophagy, necroptosis, and apoptosis, based on recent research findings and focuses on elucidating the links between PCD and diseases. Additionally, targeted therapeutic interventions for these diseases are described. This review provides original insights into the opportunities and challenges posed by current research findings. This review evaluates ways to mitigate various diseases resulting from cell death patterns. Moreover, this paper enhances the understanding of the biohazards associated with MNPs by providing a systematic reference for subsequent toxicological research and health risk mitigation efforts.

4.
Environ Pollut ; 352: 124103, 2024 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-38734053

RESUMEN

At present, the quantity of micro/nano plastics in the environment is steadily rising, and their pollution has emerged as a global environmental issue. The tendency of their bioaccumulation in aquatic organisms (especially fish) has intensified people's attention to their persistent ecotoxicology. This review critically studies the accumulation of fish in the intestines of fish through active or passive intake of micro/nano plastics, resulting in their accumulation in intestinal organs and subsequent disturbance of intestinal microflora. The key lies in the complex toxic effect on the host after the disturbance of fish intestinal microflora. In addition, this review pointed out the characteristics of micro/nano plastics and the effects of their combined toxicity with adsorbed pollutants on fish intestinal microorganisms, in order to fully understand the characteristics of micro/nano plastics and emphasize the complex interaction between MNPs and other pollutants. We have an in-depth understanding of MNPs-induced intestinal flora disorders and intestinal dysfunction, affecting the host's systemic system, including immune system, nervous system, and reproductive system. The review also underscores the imperative for future research to investigate the toxic effects of prolonged exposure to MNPs, which are crucial for evaluating the ecological risks posed by MNPs and devising strategies to safeguard aquatic organisms.


Asunto(s)
Disbiosis , Peces , Microbioma Gastrointestinal , Contaminantes Químicos del Agua , Animales , Microbioma Gastrointestinal/efectos de los fármacos , Disbiosis/inducido químicamente , Peces/microbiología , Contaminantes Químicos del Agua/toxicidad , Microplásticos/toxicidad , Plásticos , Enfermedades de los Peces/microbiología , Enfermedades de los Peces/inducido químicamente , Nanopartículas/toxicidad
5.
Fish Shellfish Immunol ; 150: 109619, 2024 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-38735599

RESUMEN

Plastic waste degrades slowly in aquatic environments, transforming into microplastics (MPs) and nanoplastics (NPs), which are subsequently ingested by fish and other aquatic organisms, causing both physical blockages and chemical toxicity. The fish immune system serves as a crucial defense against viruses and pollutants present in water. It is imperative to comprehend the detrimental effects of MPs on the fish immune system and conduct further research on immunological assessments. In this paper, the immune response and immunotoxicity of MPs and its combination with environmental pollutants on fish were reviewed. MPs not only inflict physical harm on the natural defense barriers like fish gills and vital immune organs such as the liver and intestinal tract but also penetrate cells, disrupting intracellular signaling pathways, altering the levels of immune cytokines and gene expression, perturbing immune homeostasis, and ultimately compromising specific immunity. Initially, fish exposed to MPs recruit a significant number of macrophages and T cells while activating lysosomes. Over time, this exposure leads to apoptosis of immune cells, a decline in lysosomal degradation capacity, lysosomal activity, and complement levels. MPs possess a small specific surface area and can efficiently bind with heavy metals, organic pollutants, and viruses, enhancing immune responses. Hence, there is a need for comprehensive studies on the shape, size, additives released from MPs, along with their immunotoxic effects and mechanisms in conjunction with other pollutants and viruses. These studies aim to solidify existing knowledge and delineate future research directions concerning the immunotoxicity of MPs on fish, which has implications for human health.


Asunto(s)
Peces , Microplásticos , Contaminantes Químicos del Agua , Animales , Microplásticos/toxicidad , Contaminantes Químicos del Agua/toxicidad , Peces/inmunología , Inmunidad Innata/efectos de los fármacos
6.
Environ Int ; 188: 108740, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38749117

RESUMEN

The intensification of microplastics (MPs) pollution has emerged as a formidable environmental challenge, with profound global implications. The pervasive presence of MPs across a multitude of environmental mediums, such as the atmosphere, soil, and oceans, extends to commonplace items, culminating in widespread human ingestion and accumulation via channels like food, water, and air. In the domestic realm, kitchens have become significant epicenters for MPs pollution. A plethora of kitchen utensils, encompassing coated non-stick pans, plastic cutting boards, and disposable utensils, are known to release substantial quantities of MPs particles in everyday use, which can then be ingested alongside food. This paper conducts a thorough examination of contemporary research addressing the release of MPs from kitchen utensils during usage and focuses on the health risks associated with MPs ingestion, as well as the myriad factors influencing the release of MPs in kitchen utensils. Leveraging the insights derived from this analysis, this paper proposes a series of strategic recommendations and measures targeted at mitigating the production of MPs in kitchen settings. These initiatives are designed not solely to diminish the release of MPs but also to enhance public awareness regarding this pressing environmental concern. By adopting more informed practices in kitchens, we can significantly contribute to the reduction of the environmental burden of MPs pollution, thus safeguarding both human health and the ecological system.


Asunto(s)
Microplásticos , Microplásticos/análisis , Humanos , Utensilios de Comida y Culinaria , Contaminación Ambiental , Exposición a Riesgos Ambientales , Monitoreo del Ambiente
7.
Environ Res ; 242: 117732, 2024 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-37996004

RESUMEN

As a new type of pollutant, microplastics (MPs) commonly exist in today's ecosystems, causing damage to the ecological environment and the health of biological organisms, including human beings. MPs can function as carriers of heavy metals (HMs) to aggravate the enrichment of HMs in important organs of organisms, posing a great threat to health. Ferroptosis, a novel process for the regulation of nonapoptotic cell death, has been shown to be closely related to the occurrence and processes of MPs and HMs in diseases. In recent years, some HMs, such as cadmium (Cd), iron (Fe), arsenic (As) and copper (Cu), have been proven to induce ferroptosis. MPs can function as carriers of HMs to aggravate damage to the body. This damage involves oxidative stress, mitochondrial dysfunction, lipid peroxidation (LPO), inflammation, endoplasmic reticulum stress (ERS) and so on. Therefore, ferroptosis has great potential as a therapeutic target for diseases induced by MPs combined with HMs. This paper systematically reviews the potential effects and regulatory mechanisms of MPs and HMs in the process of ferroptosis, focusing on the mitochondrial damage, Fe accumulation, LPO, ERS and inflammation caused by MPs and HMs that affect the regulatory mechanism of ferroptosis, providing new insights for research on regulating drugs and for the development of ferroptosis-targeting therapy for Alzheimer's disease, Parkinson's disease, cancer and cardiovascular disease.


Asunto(s)
Arsénico , Ferroptosis , Metales Pesados , Humanos , Microplásticos , Plásticos , Ecosistema , Metales Pesados/toxicidad , Cadmio , Inflamación
8.
Front Endocrinol (Lausanne) ; 14: 1230168, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37670891

RESUMEN

As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities.


Asunto(s)
Diabetes Mellitus Tipo 2 , Humanos , Dinámicas Mitocondriales , Apoptosis , Homeostasis , Mitocondrias
9.
J Environ Manage ; 345: 118702, 2023 Nov 01.
Artículo en Inglés | MEDLINE | ID: mdl-37536135

RESUMEN

The health damage caused by nanoplastics (NPs) pollution has become one of the global scientific problems to be solved urgently. However, the toxicological mechanism of NPs is complex, and the research progress of anti-toxicity is limited. Thus, it has potential application value to explore or develop drugs that can effectively alleviate or remove NPs with biological toxicity. In this research, 8 µM sodium nitroprusside (SNP) solution was used to treat zebrafish larvae with 20 mg/L NPs for up to 12 days, and the results showed that SNP treatments were effective in alleviating NPs-caused developmental toxicity in zebrafish larvae. Further examination of its signaling pathway revealed that NPs-induced oxidative stress was mitigated by activating the NO-sGC-cGMP signaling pathway and reduced most of the reactive oxygen species (ROS). Subsequently, we detected the key substances and the key enzymes involved in apoptosis and ferroptosis, and found that oxidative stress-induced mitochondria-dependent apoptosis and lipid peroxidation-caused ferroptosis were alleviated. Finally, observed the accumulation of NPs and ROS in the liver of zebrafish larvae, which is the target organ of immunotoxicity, and we found that SNP could alleviate NPs-caused inflammation by analyzing the fluorescence intensity of neutrophils and macrophages in transgenic zebrafish and detecting the expression of key immune genes. In conclusion, this research has shown for the first time that SNP treatment can significantly inhibit NPs-induced developmental toxicity, resulting from oxidative stress-induced apoptosis, ferroptosis and inflammation in zebrafish larvae.


Asunto(s)
Ferroptosis , Animales , Especies Reactivas de Oxígeno , Pez Cebra/metabolismo , Nitroprusiato/farmacología , Microplásticos/metabolismo , Microplásticos/farmacología , Estrés Oxidativo/genética , Apoptosis/genética , Inflamación/inducido químicamente
10.
Toxics ; 11(6)2023 May 28.
Artículo en Inglés | MEDLINE | ID: mdl-37368590

RESUMEN

Fish not only constitute an important trophic level in aquatic ecosystems but also serve as an important source of protein for human beings. The health of fish is related to the sustained and healthy development of their entire aquatic ecosystem. Due to the widespread use, mass production, high disposal frequency, and degradation resistance of plastics, these pollutants are released into aquatic environments on a large scale. They have become one of the fastest growing pollutants and have a substantial toxic effect on fish. Microplastics have intrinsic toxicity and can absorb heavy metals discharged into water. The adsorption of heavy metals onto microplastics in aquatic environments is affected by many factors and serves as a convenient way for heavy metals to migrate from the environment to organisms. Fish are exposed to both microplastics and heavy metals. In this paper, the toxic effects of heavy metal adsorption by microplastics on fish are reviewed, and the focus is on the toxic effects at the individual (survival, feeding activity and swimming, energy reserves and respiration, intestinal microorganisms, development and growth, and reproduction), cellular (cytotoxicity, oxidative damage, inflammatory response, neurotoxicity, and metabolism) and molecular (gene expression) levels. This facilitates an assessment of the pollutants' impact on ecotoxicity and contributes to the regulation of these pollutants in the environment.

11.
Int J Mol Sci ; 24(6)2023 Mar 08.
Artículo en Inglés | MEDLINE | ID: mdl-36982274

RESUMEN

Diabetes is a metabolic disease characterized by high blood glucose levels. With economic development and lifestyle changes, the prevalence of diabetes is increasing yearly. Thus, it has become an increasingly serious public health problem in countries around the world. The etiology of diabetes is complex, and its pathogenic mechanisms are not completely clear. The use of diabetic animal models is helpful in the study of the pathogenesis of diabetes and the development of drugs. The emerging vertebrate model of zebrafish has many advantages, such as its small size, large number of eggs, short growth cycle, simple cultivation of adult fish, and effective improvement of experimental efficiency. Thus, this model is highly suitable for research as an animal model of diabetes. This review not only summarizes the advantages of zebrafish as a diabetes model, but also summarizes the construction methods and challenges of zebrafish models of type 1 diabetes, type 2 diabetes, and diabetes complications. This study provides valuable reference information for further study of the pathological mechanisms of diabetes and the research and development of new related therapeutic drugs.


Asunto(s)
Diabetes Mellitus Tipo 1 , Diabetes Mellitus Tipo 2 , Hiperglucemia , Animales , Pez Cebra , Diabetes Mellitus Tipo 2/complicaciones , Modelos Animales de Enfermedad , Hiperglucemia/complicaciones , Diabetes Mellitus Tipo 1/complicaciones
12.
Front Physiol ; 13: 993904, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-36225311

RESUMEN

Worldwide, the rapid increase in the incidence of diabetes and its complications poses a serious threat to human health. Ferroptosis, which is a new nonapoptotic form of cell death, has been proven to be closely related to the occurrence and development of diabetes and its complications. In recent years, lncRNAs have been confirmed to be involved in the occurrence and development of diabetes and play an important role in regulating ferroptosis. An increasing number of studies have shown that lncRNAs can affect the occurrence and development of diabetes and its complications by regulating ferroptosis. Therefore, lncRNAs have great potential as therapeutic targets for regulating ferroptosis-mediated diabetes and its complications. This paper reviewed the potential impact and regulatory mechanism of ferroptosis on diabetes and its complications, focusing on the effects of lncRNAs on the occurrence and development of ferroptosis-mediated diabetes and its complications and the regulation of ferroptosis-inducing reactive oxygen species, the key ferroptosis regulator Nrf2 and the NF-κB signaling pathway to provide new therapeutic strategies for the development of lncRNA-regulated ferroptosis-targeted drugs to treat diabetes.

13.
Toxics ; 10(10)2022 Oct 19.
Artículo en Inglés | MEDLINE | ID: mdl-36287901

RESUMEN

Large amounts of enriched cadmium (Cd) in the environment seriously threatens the healthy and sustainable development of the aquaculture industry and greatly restricts the development of the food processing industry. Studying the distribution and toxic effects of Cd in fish, as well as the possible toxic effects of Cd on the human body, is very significant. A large number of studies have shown that the accumulation and distribution of Cd in fish are biologically specific, cause tissue differences, and seriously damage the integrity of tissue structure and function, the antioxidant defense system, the reproductive regulation system, and the immune system. The physiological, biochemical, enzyme, molecular, and gene expression levels change with different concentrations and times of Cd exposure, and these changes are closely related to the target sites of Cd action and tissues in fish. Therefore, the toxic effects of Cd on fish occur with multiple tissues, systems, and levels.

14.
Life Sci ; 310: 121015, 2022 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-36179818

RESUMEN

BACKGROUND: Diabetes mellitus (DM) is an endocrine and metabolic disease caused by a variety of pathogenic factors, including genetic factors, environmental factors and behavior. In recent decades, the number of cases and the prevalence of diabetes have steadily increased, and it has become one of the most threatening diseases to human health in the world. Currently, insulin is the most effective and direct way to control hyperglycemia for diabetes treatment at a low cost. However, hypoglycemia is often a common complication of insulin treatment. Moreover, with the extension of treatment time, insulin resistance, considered the typical adverse symptom, can appear. Therefore, it is urgent to develop new targets and more effective and safer drugs for diabetes treatment to avoid adverse reactions and the insulin tolerance of traditional hypoglycemic drugs. SCOPE OF REVIEW: In recent years, it has been found that some fibroblast growth factors (FGFs), including FGF1, FGF19 and FGF21, can safely and effectively reduce hyperglycemia and have the potential to be developed as new drugs for the treatment of diabetes. FGF23 is also closely related to diabetes and its complications, which provides a new approach for regulating blood glucose and solving the problem of insulin tolerance. MAJOR CONCLUSIONS: This article reviews the research progress on the physiology and pharmacology of fibroblast growth factor in the treatment of diabetes. We focus on the application of FGFs in diabetes care and prevention.


Asunto(s)
Diabetes Mellitus , Factores de Crecimiento de Fibroblastos , Hiperglucemia , Humanos , Glucemia/metabolismo , Diabetes Mellitus/tratamiento farmacológico , Factores de Crecimiento de Fibroblastos/uso terapéutico , Hiperglucemia/tratamiento farmacológico , Insulina/uso terapéutico
15.
Drug Des Devel Ther ; 16: 2707-2728, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35996567

RESUMEN

Skin injuries caused by accidents and acute or chronic diseases place a heavy burden on patients and health care systems. Current treatments mainly depend on preventing infection, debridement, and hemostasis and on supplementing growth factors, but patients will still have scar tissue proliferation or difficulty healing and other problems after treatment. Conventional treatment usually focuses on a single factor or process of wound repair and often ignores the influence of the wound pathological microenvironment on the final healing effect. Therefore, it is of substantial research value to develop multifunctional therapeutic methods that can actively regulate the wound microenvironment and reduce the oxidative stress level at the wound site to promote the repair of skin wounds. In recent years, various bioactive nanomaterials have shown great potential in tissue repair and regeneration due to their properties, including their unique surface interface effect, small size effect, enzyme activity and quantum effect. This review summarizes the mechanisms underlying skin wound repair and the defects in traditional treatment methods. We focus on analyzing the advantages of different types of nanomaterials and comment on their toxicity and side effects when used for skin wound repair.


Asunto(s)
Nanoestructuras , Cicatrización de Heridas , Hemostasis , Humanos , Piel/patología , Cicatrización de Heridas/fisiología
16.
Gene ; 835: 146656, 2022 Aug 15.
Artículo en Inglés | MEDLINE | ID: mdl-35680025

RESUMEN

Gallinacin-3 (Gal-3) is a newly discovered epithelial beta-defensin that acts as cationic antimicrobial peptides, and plays an important role in chicken innate immunity. However, the gallinacin-3 precursor containeda lengthy C-terminal region, which often hindered itsexpression. After codon optimization of Gal-3 and construction of an expression vector, the transgenic plants of Medicago sativa were obtained. Transgenic plants were validated and expression of proteins was detected. The antimicrobial activity of chicken ß Gal-3 was analyzed and effects of chicken ß Gal-3 on the body weight and intestinal microflora of mice were described. Our results demonstrated that the codon optimized chicken Gal-3 was stably expressed in transgenic Medicago sativa using the pCAMBIA3301 expression vector under the control of protein phosphatase (Ppha) promoter. Five transgenic plants with the highest expression of chicken ß Gal-3 were selected, and were evaluated for the in vitro antimicrobial activity against Escherichia coli, Staphylococcus aureus and Salmonella typhi. Our findings confirmed that the Minimum Inhibitory Concentration (MIC) of the three bacterial strains were 32, 16 and 128 µg/mL, respectively. In addition, the effect of chicken Gal-3 on the body weight of mice fed with transgenic plants showed no significant deviation compared with that of the control group. Similarly, no loss of intestinal microflora was evident in the experimental group compared with the control group. Together, our findings demonstrate an alternative method for the stable expression of chicken Gal-3 withsignificant antibacterial effects and potential probiotics uses. In addition, this study may also be useful in the development of resistant M. sativa plants against pathogenic bacteria in future studies.


Asunto(s)
Antiinfecciosos , Pollos , Galectinas/metabolismo , Animales , Antibacterianos/farmacología , Peso Corporal/genética , Pollos/genética , Codón , Escherichia coli/genética , Medicago sativa/genética , Ratones , Plantas Modificadas Genéticamente/genética
17.
Apoptosis ; 27(7-8): 509-520, 2022 08.
Artículo en Inglés | MEDLINE | ID: mdl-35596834

RESUMEN

In recent decades, diabetes mellitus has become a major chronic disease threatening human health worldwide, and the age of patients tends to be younger; however, the pathogenesis remains unclear, resulting in many difficulties in its treatment. As an ideal model animal, zebrafish can simulate the processes of human diabetes well. In this study, we successfully established a model of diabetic zebrafish larvae in a previous work. Furthermore, transcriptome analysis was completed, and the results suggested that 10.59% of differentially expressed genes (DEGs) related to the apoptosis pathway need to be considered. Then, glucose-induced developmental toxicity, reactive oxygen species (ROS) accumulation, antioxidant system function, apoptosis and mitochondrial dysfunction were measured in zebrafish larvae. We hope that this study will provide valuable reference information for type 2 juvenile diabetes treatment.


Asunto(s)
Apoptosis , Pez Cebra , Animales , Embrión no Mamífero/metabolismo , Glucosa/metabolismo , Glucosa/farmacología , Humanos , Larva/metabolismo , Mitocondrias/metabolismo , Estrés Oxidativo , Especies Reactivas de Oxígeno/metabolismo
18.
Ecotoxicol Environ Saf ; 239: 113666, 2022 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-35605332

RESUMEN

Hydrogen sulfide (H2S), a highly toxic gas, has become a polluting gas that cannot be ignored, while H2S exposure results in acute or chronic poisoning or even death in humans or animals and plants, but the relevant mechanisms remain poorly understood. In this study, 9-day-old zebrafish larvae were exposed continuously to culture medium containing 30 µM survival rate was counted on H2S, and our results indicated that H2S exposure increased intracellular ROS, Ca2+, NO and MDA contents and decreased SOD activity, meaning that H2S caused oxidative stress in embryo-larval stages of zebrafish. Furthermore, we found that transgenic zebrafish (cms Tg/+ AB) displayed a lower fluorescence intensity, and cytochrome c oxidase (COX) activity and JC-1 monomer fluorescence ratio increased under H2S treatment conditions. These findings indicated that H2S caused mitochondrial dysfunction. Moreover, in this experiment, after H2S treatment, the increase of apoptotic cells, activity of caspase 3 and transcription of typical apoptosis-associated genes including BCL2 associated agonist of cell death (Bad), and BCL2 associated X apoptosis (Baxa) and so on were found, which suggested that H2S caused apoptosis in zebrafish larvae. Therefore, our data meant that H2S-traggered oxidative stress mediate mitochondrial dysfunction, thus triggering apoptosis. In conclusion, oxidative stress triggered H2S-induced apoptosis via mitochondria pathway in embryo-larval stages of zebrafish.


Asunto(s)
Apoptosis , Sulfuro de Hidrógeno , Mitocondrias , Estrés Oxidativo , Animales , Sulfuro de Hidrógeno/efectos adversos , Larva/metabolismo , Mitocondrias/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Pez Cebra/metabolismo
19.
Plants (Basel) ; 11(10)2022 May 19.
Artículo en Inglés | MEDLINE | ID: mdl-35631776

RESUMEN

Plants have evolved many strategies for adaptation to extreme environments. Ca2+, acting as an important secondary messenger in plant cells, is a signaling molecule involved in plants' response and adaptation to external stress. In plant cells, almost all kinds of abiotic stresses are able to raise cytosolic Ca2+ levels, and the spatiotemporal distribution of this molecule in distant cells suggests that Ca2+ may be a universal signal regulating different kinds of abiotic stress. Ca2+ is used to sense and transduce various stress signals through its downstream calcium-binding proteins, thereby inducing a series of biochemical reactions to adapt to or resist various stresses. This review summarizes the roles and molecular mechanisms of cytosolic Ca2+ in response to abiotic stresses such as drought, high salinity, ultraviolet light, heavy metals, waterlogging, extreme temperature and wounding. Furthermore, we focused on the crosstalk between Ca2+ and other signaling molecules in plants suffering from extreme environmental stress.

20.
Pharmaceutics ; 13(9)2021 Sep 11.
Artículo en Inglés | MEDLINE | ID: mdl-34575528

RESUMEN

Over the past decade, ROS-sensitive formulations have been widely used in atherosclerosis applications such as ROS scavenging, drug delivery, gene delivery, and imaging. The intensified interest in ROS-sensitive formulations is attributed to their unique self-adaptive properties, involving the main molecular mechanisms of solubility switch and degradation under the pathological ROS differences in atherosclerosis. This review outlines the advances in the use of ROS-sensitive formulations in atherosclerosis applications during the past decade, especially highlighting the general design requirements in relation to biomedical functional performance.

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