Effects of Di-2-ethylhexyl phthalate on central nervous system functions: A narrative review

2021 ◽  
Vol 19 ◽  
Author(s):  
Soheila Safarpour ◽  
Maryam Ghasemi–Kasman ◽  
Samaneh Safarpour ◽  
Yasaman Mahdizadeh Darban
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Memory Loss ◽  
Review Article ◽  
Low Doses ◽  
Endocrine Glands ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure ◽  
Plastics Industry ◽  
High Absorption

Background: Di-2-Ethylhexyl phthalate (DEHP) is one of the essential phthalate metabolites that disrupt the function of endocrine glands and causes numerous effects on animals, humans, and the environment. Phthalates are widely used in the plastics industry. Low doses of DEHP increase neurotoxicity in the nervous system that has arisen deep concerns due to the widespread nature of DEHP exposure and its high absorption during brain development. Objective: This review article evaluated the impacts of DEHP exposure from birth to adulthood on neurobehavioral damages. Then, the possible mechanisms of DEHP-induced neurobehavioral impairment were discussed. Methodology: Peer-reviewed articles were extracted through Embase, PubMed, and Google Scholar till the year 2021. Results: The results showed that exposure to DEHP during pregnancy and infancy leads to memory loss and irreversible nervous system damage. Conclusion: Overall, it seems that increased levels of oxidative stress and inflammatory mediators possess a pivotal role in DEHP-induced neurobehavioral impairment.

scholarly journals Low Doses of Imidacloprid Induce Oxidative Stress and Neural Cell Disruption in Earthworm Eisenia fetida

2021 ◽  
Vol 84 ◽  
pp. 1-11
Author(s):  
Artem Huslystyi ◽  
Victor Nedzvetsky ◽  
Serhii Yermolenko ◽  
Viktor Gasso ◽  
Vladyslav Petrushevskyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuron Specific Enolase ◽  
Stress Generation ◽  
Low Doses ◽  
Neuronal Marker ◽  
Dose Dependent Decrease ◽  
Species Production ◽  
Dose Dependent

Imidacloprid is a widely used pesticide that belongs to the class of neonicotinoids. There is a piece of rising evidence that neonicotinoids exert cytotoxic effects in non-target organisms including vertebrate species such as mammals. Nevertheless, dose-limiting toxicity and molecular mechanisms of neonicotinoids' deleterious effects are still poorly understood. In accord to imidacloprid fate in the environment, the most of used pesticide is absorbed in the soil. Therefore, earthworms, which are prevailing soil organisms, could be considered as a target of neonicotinoids toxicity. The earthworm’s simple nervous system is a prospective model for neurotoxicological studies. We exposed earthworms to imidacloprid in a paper contact test with a doses range of 0.1‑0.4 µg/cm2 for 14 days. In the present work, we studied the imidacloprid effect on oxidative stress generation and neuronal marker neuron-specific enolase (NSE) expression. The exposure to imidacloprid induced a dose-dependent decrease in NSE. Both reactive oxygen species production and lipid peroxidation level were upregulated as well. Observed NSE decline suggests imidacloprid-caused disturbance in earthworm neuron cells. Obtained data have shown that relatively low doses of imidacloprid are potent to induce cytotoxicity in neurons. Furthermore, neurotoxicity could be recognized as one of an individual scenario of the general imidacloprid toxicity. Thus, presented results suggest the cytotoxicity of imidacloprid low doses in non-target organisms and hypothesize that NSE downregulation could be estimated as a biomarker of neonicotinoid cytotoxicity in a nervous system of non-insect species.

Di(2-ethylhexyl)phthalate induces reproductive toxicity via JAZF1/TR4 pathway and oxidative stress in pubertal male rats

2019 ◽  
Vol 35 (3) ◽  
pp. 228-238 ◽  
Author(s):  
Yu-Qin Shi ◽  
Guo-Qing Fu ◽  
Jing Zhao ◽  
Shen-Zhou Cheng ◽  
You Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Reproductive Toxicity ◽  
Male Reproduction ◽  
Male Rats ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Cyclin A1 ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure ◽  
And Oxidative Stress

Di(2-ethylhexyl)phthalate (DEHP) is a typical endocrine-disrupting chemical and reproductive toxicant. Although previous studies have attempted to describe the mechanism by which DEHP exposure results in reproductive dysfunction, few studies focused on puberty, a critical period of reproductive development, and the increased susceptibility to injury in adolescents. To elucidate the mechanism underpinning the testicular effects of DEHP in puberty, we sought to investigate the JAZF1/TR4 pathway in the testes of pubertal rats. Specifically, we focused on the role of the JAZF1/TR4 pathway in male reproduction, including the genes JAZF1, TR4, Sperm 1, and Cyclin A1. In the present study, rats were exposed to increasing concentrations of DEHP (0, 250, 500, and 1000 mg/kg/day) by oral gavages for 30 days. Then we assayed testicular zinc and oxidative stress levels. Our results indicated that DEHP exposure could lead to oxidative stress and decrease the contents of testicular zinc. Additionally, significant morphological changes and cell apoptosis were observed in testes exposed to DEHP, as identified by hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated nick and labeling assay. By measuring the expression levels of the above relevant genes by qPCR, we found the DEHP-induced increased expression of JAZF1 and decreased expression of TR4, Sperm 1, and Cyclin A1. Therefore, we have demonstrated that in vivo exposure to DEHP might induce reproductive toxicity in pubertal male rats through the JAZF1/TR4 pathway and oxidative stress.

scholarly journals THERAPEUTIC USES OF NASYA KARMA: CONCEPTUAL CRITICAL REVIEW

2020 ◽  
pp. 126-132
Author(s):  
Rahul Parihar ◽  
Suman Dadhich
Keyword(s):  
Nervous System ◽  
Review Article ◽  
The Body ◽  
Entire Body ◽  
Systemic Diseases ◽  
Purification Procedure ◽  
Endocrine Glands ◽  
Therapeutic Measure ◽  
Therapeutic Uses ◽  
Diseased Condition

Nasa (Nose) is an Indriya, which works not only to perceive the smell but also to provide the main breathing pathway, along with this, Nasa is one of the drug administration pathways. Acharyas have been placed Nasya as one of the Panchkarma procedures, which signify the importance of Nasya as Shodhana Karma (Purification procedure) especially for Urddhva-jatrugata Vikara (disease which affect the body above clavicle). Nasya Karma is a therapeutic measure in which the drug (Medicated Oil/Ghee/ Decoction/ Powder/Smoke etc.) is administered by Nasa (Nose) essentially to remove the vitiated Dosha found in Shira and its constituent parts. Indirectly, by enhancing the functions of the endocrine glands and nervous system, Nasya can operate on the entire body. In classics Nasya is mentioned in different type of supra-clavicular as well as in systemic diseases. So present review article focused on the therapeutic uses of Nasya Karma in different diseased condition which are proven by clinical researches.

scholarly journals Effects of Di-(2-Ethylhexyl) Phthalate At Environmentally Relevant Concentrations On Oxidative Stress and Lipid Metabolism in Livers of Male Xenopus Tropicalis

2021 ◽  
Author(s):  
Xinying Pan ◽  
Li Zheng ◽  
Yong Ding ◽  
Zhuo Dai ◽  
Xufeng Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Aquatic Organisms ◽  
Mitochondrial Morphology ◽  
Histopathological Analysis ◽  
Expression Of Genes ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure

Abstract Di-(2-ethylhexyl) phthalate (DEHP), used as a popular plasticizer to enhance the flexibility of plastics, is a major pollutant in aquatic environments. DEHP poses severe risks to aquatic organisms since it is an endocrine-disrupting compound. To comprehensively evaluate the toxicity of DEHP on the growth and livers of male X. tropicalis, sexually mature male X. tropicalis were exposed to environmentally relevant concentrations of DEHP, 0.2, 0.6, 1.8, 5.4 mg/L, for 49 days. The results showed that DEHP had a severe toxic effect on the livers of male X. tropicalis. Histopathological analysis of livers in all the DEHP-exposed groups showed changes in terms of vacuolization, loose cell cords, and an increasing amount of melanin. Large lipid droplets were markedly formed, and there were changes in the mitochondrial morphology upon DEHP exposure. In addition, oxidative stress was induced through the suppression of biochemical indicators and the downregulation in the mRNA expression of genes (nrf2, cat, sod, gst, and gpx) related to oxidative stress. A reduction in expression of fatty acid metabolism-related genes (pparα) was seen post-DEHP exposure. Thus, our study suggests that the hepatotoxicity induced by DEHP could be attributed to oxidative stress and disordered fatty acid metabolism. In conclusion, long-term exposure to DEHP at environmentally relevant concentrations poses ecological risks to aquatic organisms, which serves as a reminder that the application of DEHP and other plasticizers should be limited.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

Brain organoids: a promising model to assess oxidative stress‐induced Central Nervous System damage

2021 ◽  
Author(s):  
Foluwasomi A. Oyefeso ◽  
Alysson R. Muotri ◽  
Christopher G. Wilson ◽  
Michael J. Pecaut
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage

scholarly journals Non-Oncological Neuroradiological Manifestations in NF1 and Their Clinical Implications

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1831
Author(s):  
Camilla Russo ◽  
Carmela Russo ◽  
Daniele Cascone ◽  
Federica Mazio ◽  
Claudia Santoro ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Structural Organization ◽  
Neurofibromatosis Type ◽  
Review Article ◽  
Tumor Suppressor Protein ◽  
Clinical Implications ◽  
Nf1 Gene ◽  
The Central Nervous System

Neurofibromatosis type 1 (NF1), the most frequent phakomatosis and one of the most common inherited tumor predisposition syndromes, is characterized by several manifestations that pervasively involve central and peripheral nervous system structures. The disorder is due to mutations in the NF1 gene, which encodes for the ubiquitous tumor suppressor protein neurofibromin; neurofibromin is highly expressed in neural crest derived tissues, where it plays a crucial role in regulating cell proliferation, differentiation, and structural organization. This review article aims to provide an overview on NF1 non-neoplastic manifestations of neuroradiological interest, involving both the central nervous system and spine. We also briefly review the most recent MRI functional findings in NF1.

A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats

Synapse ◽  
2015 ◽  
Vol 69 (9) ◽  
pp. 421-433 ◽  
Author(s):  
Samuel Treviño ◽  
Patrícia Aguilar-Alonso ◽  
Jose Angel Flores Hernandez ◽  
Eduardo Brambila ◽  
Jorge Guevara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Temporal Cortex ◽  
Memory Loss ◽  
Calorie Diet ◽  
And Oxidative Stress ◽  
High Calorie Diet ◽  
High Calorie

scholarly journals The Role of Oxidative Stress-Induced Epigenetic Alterations in Amyloid-βProduction in Alzheimer’s Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Li Zuo ◽  
Benjamin T. Hemmelgarn ◽  
Chia-Chen Chuang ◽  
Thomas M. Best
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Treatment Options ◽  
Memory Loss ◽  
The United States ◽  
Traditional Medicines ◽  
Progressive Neurodegeneration ◽  
Antioxidant Supplements

An increasing number of studies have proposed a strong correlation between reactive oxygen species (ROS)-induced oxidative stress (OS) and the pathogenesis of Alzheimer’s disease (AD). With over five million people diagnosed in the United States alone, AD is the most common type of dementia worldwide. AD includes progressive neurodegeneration, followed by memory loss and reduced cognitive ability. Characterized by the formation of amyloid-beta (Aβ) plaques as a hallmark, the connection between ROS and AD is compelling. Analyzing the ROS response of essential proteins in the amyloidogenic pathway, such as amyloid-beta precursor protein (APP) and beta-secretase (BACE1), along with influential signaling programs of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and c-Jun N-terminal kinase (JNK), has helped visualize the path between OS and Aβoverproduction. In this review, attention will be paid to significant advances in the area of OS, epigenetics, and their influence on Aβplaque assembly. Additionally, we aim to discuss available treatment options for AD that include antioxidant supplements, Asian traditional medicines, metal-protein-attenuating compounds, and histone modifying inhibitors.

Sign in / Sign up

Export Citation Format

Share Document