Probing the biological toxicity of pyrene to the earthworm Eisenia fetida and the toxicity pathways of oxidative damage: A systematic study at the animal and molecular levels

Abstract Phenanthrene (PHE) contamination not only changes the quality of soil environment but also threatens to the soil organisms. There is lack of focus on the eco-toxicity potential of contaminants in real soil in the current investigation. Here, we assessed the toxic effects of PHE on earthworms (Eisenia fetida) in natural soil matrix. PHE exhibited a relatively high toxicity to E. fetida in natural soil, with the LC50 determined to be 56.68 mg kg−1 after a 14-day exposure. Excessive ROS induced by PHE, leading to oxidative damage to biomacromolecules in E. fetida, including lipid peroxidation, protein carbonylation, and DNA damage. The antioxidant defense system (total antioxidant capacity, glutathione S-transferase, peroxidase, catalase, carboxylesterase, and superoxide dismutase) in E. fetida responded quickly to scavenge excess ROS and free radicals. Exposure to PHE resulted in earthworm avoidance responses (2.5 mg kg−1) and habitat function loss (10 mg kg−1). Histological observations indicated that the intestine, body wall, and seminal vesicle in E. fetida were severely damaged after exposure to high-dose PHE. Moreover, earthworm growth (weight change) and reproduction (cocoon production and the number of juvenile) were also inhibited after exposure to this pollutant. Furthermore, the integrated toxicity of PHE toward E. fetida at different doses and exposure times was assessed by the integrated biomarker response (IBR), which confirm that PHE is more toxic to earthworms in the high-dose and long-term exposure groups. Our results showed that PHE exposure induced oxidative stress, disturbed antioxidant defense system, and caused oxidative damage in E. fetida. These effects can trigger behavior changes and damaged histological structure, finally cause growth inhibition, genotoxicity, and reproductive toxicity in earthworms. The strength of this study is the comprehensive toxicity evaluation of PHE to earthworms and highlights the need to investigate the t eco-toxicity potential of exogenous environmental pollutants in a real soil environment.

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Toxic effect of [Omim]BF 4 and [Omim]Br on antioxidant stress and oxidative damage in earthworms ( Eisenia fetida )

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2018.04.008 ◽

2018 ◽

Vol 60 ◽

pp. 37-44 ◽

Cited By ~ 13

Author(s):

Yuting Shao ◽

Jun Wang ◽

Zhongkun Du ◽

Bing Li ◽

Lusheng Zhu ◽

...

Keyword(s):

Oxidative Damage ◽

Toxic Effect ◽

Eisenia Fetida ◽

Antioxidant Stress

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Oxidative Damage and Genetic Toxicity Induced by DBP in Earthworms (Eisenia fetida)

Archives of Environmental Contamination and Toxicology ◽

10.1007/s00244-017-0451-4 ◽

2017 ◽

Vol 74 (4) ◽

pp. 527-538 ◽

Cited By ~ 13

Author(s):

Guanying Wang ◽

Jun Wang ◽

Lusheng Zhu ◽

Jinhua Wang ◽

Hengzhou Li ◽

...

Keyword(s):

Oxidative Damage ◽

Eisenia Fetida ◽

Genetic Toxicity

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Erythrophagocytosis in the Liver in Hemolytic Anemias

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100100664 ◽

1968 ◽

Vol 26 ◽

pp. 184-185

Author(s):

O. T. Minick ◽

E. Orfei ◽

F. Volini ◽

G. Kent

Keyword(s):

Acid Phosphatase ◽

Oxidative Damage ◽

Phosphatase Activity ◽

Kupffer Cells ◽

Acid Phosphatase Activity ◽

Common Type ◽

Red Cell ◽

Cell Fragments ◽

Reticulo Endothelial System ◽

Important Site

Hemolytic anemias were produced in rats by administering phenylhydrazine or anti-erythrocytic (rooster) serum, the latter having agglutinin and hemolysin titers exceeding 1:1000.Following administration of phenylhydrazine, the erythrocytes undergo oxidative damage and are removed from the circulation by the cells of the reticulo-endothelial system, predominantly by the spleen. With increasing dosage or if animals are splenectomized, the Kupffer cells become an important site of sequestration and are greatly hypertrophied. Whole red cells are the most common type engulfed; they are broken down in digestive vacuoles, as shown by the presence of acid phosphatase activity (Fig. 1). Heinz body material and membranes persist longer than native hemoglobin. With larger doses of phenylhydrazine, erythrocytes undergo intravascular fragmentation, and the particles phagocytized are now mainly red cell fragments of varying sizes (Fig. 2).

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Quantitative parallel EELS spectrum imaging developed as a new tool in AEM

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010013064x ◽

1992 ◽

Vol 50 (2) ◽

pp. 1202-1203

Author(s):

Gianluigi Botton ◽

Gilles L'espérance

Keyword(s):

Statistical Analysis ◽

Spatial Resolution ◽

Personal Computer ◽

Systematic Study ◽

Present Author ◽

Chemical Elements ◽

Detection Limits ◽

Research Groups ◽

Quantitative Performance ◽

Spectrum Imaging

As interest for parallel EELS spectrum imaging grows in laboratories equipped with commercial spectrometers, different approaches were used in recent years by a few research groups in the development of the technique of spectrum imaging as reported in the literature. Either by controlling, with a personal computer both the microsope and the spectrometer or using more powerful workstations interfaced to conventional multichannel analysers with commercially available programs to control the microscope and the spectrometer, spectrum images can now be obtained. Work on the limits of the technique, in terms of the quantitative performance was reported, however, by the present author where a systematic study of artifacts detection limits, statistical errors as a function of desired spatial resolution and range of chemical elements to be studied in a map was carried out The aim of the present paper is to show an application of quantitative parallel EELS spectrum imaging where statistical analysis is performed at each pixel and interpretation is carried out using criteria established from the statistical analysis and variations in composition are analyzed with the help of information retreived from t/γ maps so that artifacts are avoided.

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Protective effect of chitooligosaccharides on hydrogen peroxide-induced PC-12 cells death by inhibition of oxidative damage

Cell Biology International ◽

10.1042/cbi034s027d ◽

2010 ◽

Vol 34 (8) ◽

pp. S27-S27

Author(s):

Xueling Dai ◽

Ping Chang ◽

Ke Xu ◽

Changjun Lin ◽

Hanchang Huang ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Oxidative Damage ◽

Protective Effect ◽

Pc 12 Cells ◽

Cells Death

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Aging and Oxidative Damage: Are Telomeres the Target?

Comments® on Theoretical Biology ◽

10.1080/08948550214391 ◽

2002 ◽

Vol 7 (5) ◽

pp. 295-313 ◽

Cited By ~ 1

Author(s):

Patricia A. McChesney ◽

Lynne W. Elmore ◽

Shawn E. Holt

Keyword(s):

Oxidative Damage

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Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000628 ◽

2019 ◽

pp. 1-7 ◽

Cited By ~ 1

Author(s):

Paulina Iwan ◽

Jan Stepniak ◽

Malgorzata Karbownik-Lewinska

Keyword(s):

Lipid Peroxidation ◽

Oxidative Damage ◽

Membrane Lipids ◽

Chemical Properties ◽

Iodine Concentration ◽

Free Radical Scavenger ◽

Radical Scavenger ◽

Protective Effects ◽

Potassium Iodate ◽

Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

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Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

VASA ◽

10.1024/0301-1526/a000621 ◽

2017 ◽

Vol 46 (4) ◽

pp. 268-274

Author(s):

Erhan Saraçoğlu ◽

Ertan Vuruşkan ◽

Yusuf Çekici ◽

Salih Kiliç ◽

Halil Ay ◽

...

Keyword(s):

Oxidative Stress ◽

Carotid Artery ◽

Oxidative Damage ◽

Carotid Artery Stenosis ◽

Artery Stenosis ◽

Oxidative Stress Marker ◽

Asymptomatic Carotid ◽

Imaging Methods ◽

Neurological Findings ◽

Asymptomatic Carotid Artery Stenosis

Abstract. Background: After carotid artery stenting (CAS), neurological complications that cannot be explained with imaging methods may develop. In our study we aimed to show, using oxidative stress markers, isolated oxidative damage and resulting neurological findings following CAS in patients with asymptomatic carotid artery stenosis. Patients and methods: We included 131 neurologically asymptomatic patients requiring CAS. The neurological findings were evaluated using the modified Rankin Scale (mRS) prior to the procedure, one hour post-procedure, and two days after. Patients with elevated mRS scores but with or without typical hyperintense lesions observed on an MRI and with changes of oxidative stress marker levels at the time (Δtotal-thiol, Δtotal antioxidative status [TAS], and Δtotal oxidant status [TOS]) were evaluated. Results: In the neurological examination carried out one hour prior to the procedure, there were 92 patients with mRS = 0, 20 with mRS = 1, and 12 with mRS = 2. When Δtotal-thiol, ΔTAS, and ΔTOS values and the mRS were compared, it was observed that as the difference in oxidative parameters increased, clinical deterioration also increased proportionally (p = 0.001). Conclusions: We demonstrate a possible correlation between oxidative damage and neurological findings after CAS which could not be explained by routine imaging methods.

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