scholarly journals Antioxidant Response and Oxidative Stress in the Respiratory Tree of Sea Cucumber (Apostichopus japonicus) Following Exposure to Crude Oil and Chemical Dispersant

2020 ◽  
Vol 8 (8) ◽  
pp. 547 ◽  
Author(s):  
Xishan Li ◽  
Guoxiang Liao ◽  
Zhonglei Ju ◽  
Chengyan Wang ◽  
Nan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Crude Oil ◽  
Sea Cucumber ◽  
Oil Spills ◽  
Apostichopus Japonicus ◽  
Antioxidant Response ◽  
Chemical Dispersant ◽  
Respiratory Tree ◽  
And Oxidative Stress

Sea cucumber (Apostichopus japonicus) is mainly cultured in the coastal zone, where it is easily threatened by accidental oil spills. Chemical dispersant is one of the efficient oil spill responses for mitigating the overall environmental damage of oil spills. However, the impact of crude oil and chemical dispersants on sea cucumber is less well known. Hence, the present study focused on exploring the antioxidant response and oxidative stress in the respiratory tree of sea cucumber following exposure to GM-2 chemical dispersant (DISP), water-accommodated fractions (WAF), and chemically enhanced WAF (CEWAF) of Oman crude oil for 24 h. Results manifested that WAF exposure caused a significant increase in the reactive oxygen species (ROS) level (5.29 ± 0.30 AU·mgprot−1), and the effect was much more obvious in CEWAF treatment (5.73 ± 0.16 AU·mgprot−1). Total antioxidant capacity (T-AOC), as an important biomarker of the antioxidant defense capacity, showed an increasing trend following WAF exposure (0.95 ± 0.12 U·mgprot−1) while a significant reduction in T-AOC was observed following CEWAF exposure (0.23 ± 0.13 U·mgprot−1). Moreover, we also evaluated the oxidative damage of the macromolecules (DNA, protein, and lipid), and our results revealed that the presence of chemical dispersant enhanced oxidative damage caused by crude oil to sea cucumber.

scholarly journals Effects of Acute and Chronic Exposure to Semicarbazide on the Sea Cucumber Apostichopus japonicus

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiuhui Tian ◽  
Huanjun Li ◽  
Xiuzhen Zhang ◽  
Yingjiang Xu ◽  
Huawei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Exposure ◽  
Sea Cucumber ◽  
Intestinal Tract ◽  
Longitudinal Muscle ◽  
Apostichopus Japonicus ◽  
Lethal Concentration ◽  
Protein Digestion ◽  
Respiratory Tree ◽  
Acute And Chronic Exposure

The effects of acute and chronic exposure to semicarbazide were carried out on the sea cucumber Apostichopus japonicus. A half-maximal lethal concentration of 3.72 g/L of semicarbazide hydrochloride (95% confidence interval 3.43–4.02 g/L) was deduced. At 20, 4, and 2% of the half-maximal lethal concentrations, a 28-days exposure induced morphological alterations, oxidative stress, and acetylcholinesterase (AChE) activity in the respiratory tree, intestinal tract, and longitudinal muscle of A. japonicus. Exposure to 20% of the half-maximal lethal concentration resulted in lesions in the respiratory tree and disintegration in the intestinal tract. Exposure to lower concentration induced a gradual accumulation of lesions in the respiratory tree, intestinal tract, and longitudinal muscle. Levels of markers of oxidative stress and neurotransmission, including superoxide dismutase (SOD), catalase, and AChE, were increased during the initial days of exposure and then decreased. The activity of SOD, catalase, and AChE were highest in A. japonicus exposed to 4%, followed by 20 and 2% of the half-maximal lethal concentration at the same time. At the later stages of the 28-days exposure, marker levels were decreased and close to levels in the control groups. Non-targeted metabolomics indicated that significantly different metabolites were screened out, 28 in the positive ion mode and 38 in the negative ion mode, impairments in neurological function, osmotic pressure regulation, energy metabolism, and protein digestion and absorption following exposure of A. japonicus to semicarbazide. KEGG pathway enrichment showed that the exposure affected pathways related to ABC transporters, central carbon metabolism in cancer, protein digestion and absorption, aminoacyl-tRNA biosynthesis, and biosynthesis of unsaturated fatty acids.

scholarly journals Combined Effects of Elevated Temperature and Crude Oil Pollution on Oxidative Stress and Apoptosis in Sea Cucumber (Apostichopus japonicus, Selenka)

2021 ◽  
Vol 18 (2) ◽  
pp. 801
Author(s):  
Xishan Li ◽  
Chengyan Wang ◽  
Nan Li ◽  
Yali Gao ◽  
Zhonglei Ju ◽  
...  
Keyword(s):  
Elevated Temperature ◽  
Oxidative Damage ◽  
Crude Oil ◽  
Sea Cucumber ◽  
Oil Pollution ◽  
Apostichopus Japonicus ◽  
Global Climate ◽  
Combined Effects ◽  
Water Accommodated Fractions ◽  
Cellular Apoptosis

Currently, global climate change and oil pollution are two main environmental concerns for sea cucumber (Apostichopus japonicus) aquaculture. However, no study has been conducted on the combined effects of elevated temperature and oil pollution on sea cucumber. Therefore, in the present study, we treated sea cucumber with elevated temperature (26 °C) alone, water-accommodated fractions (WAF) of Oman crude oil at an optimal temperature of 16 °C, and Oman crude oil WAF at an elevated temperature of 26 °C for 24 h. Results showed that reactive oxygen species (ROS) level and total antioxidant capacity in WAF at 26 °C treatment were higher than that in WAF at 16 °C treatment, as evidenced by 6.03- and 1.31-fold-higher values, respectively. Oxidative damage assessments manifested that WAF at 26 °C treatment caused much severer oxidative damage of the biomacromolecules (including DNA, proteins, and lipids) than 26 °C or WAF at 16 °C treatments did. Moreover, compared to 26 °C or WAF at 16 °C treatments, WAF at 26 °C treatment induced a significant increase in cellular apoptosis by detecting the caspase-3 activity. Our results revealed that co-exposure to elevated temperature and crude oil could simulate higher ROS levels and subsequently cause much severer oxidative damage and cellular apoptosis than crude oil alone on sea cucumber.

scholarly journals Sperm motility characteristics and oxidative stress in crude oil exposed rats

2018 ◽  
Vol 110 (4) ◽  
pp. e173
Author(s):  
S.A. Bamiro ◽  
S.O. Elias ◽  
L.C. Ajonuma
Keyword(s):  
Oxidative Stress ◽  
Crude Oil ◽  
Sperm Motility ◽  
And Oxidative Stress

scholarly journals Centella asiatica Attenuates Mitochondrial Dysfunction and Oxidative Stress in Aβ-Exposed Hippocampal Neurons

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Nora E. Gray ◽  
Jonathan A. Zweig ◽  
Donald G. Matthews ◽  
Maya Caruso ◽  
Joseph F. Quinn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Neuroblastoma Cells ◽  
Water Extract ◽  
Centella Asiatica ◽  
Antioxidant Response ◽  
And Oxidative Stress

Centella asiatica has been used for centuries to enhance memory. We have previously shown that a water extract of Centella asiatica (CAW) protects against the deleterious effects of amyloid-β (Aβ) in neuroblastoma cells and attenuates Aβ-induced cognitive deficits in mice. Yet, the neuroprotective mechanism of CAW has yet to be thoroughly explored in neurons from these animals. This study investigates the effects of CAW on neuronal metabolism and oxidative stress in isolated Aβ-expressing neurons. Hippocampal neurons from amyloid precursor protein overexpressing Tg2576 mice and wild-type (WT) littermates were treated with CAW. In both genotypes, CAW increased the expression of antioxidant response genes which attenuated the Aβ-induced elevations in reactive oxygen species (ROS) and lipid peroxidation in Tg2576 neurons. CAW also improved mitochondrial function in both genotypes and increased the expression of electron transport chain enzymes and mitochondrial labeling, suggesting an increase in mitochondrial content. These data show that CAW protects against mitochondrial dysfunction and oxidative stress in Aβ-exposed hippocampal neurons which could contribute to the beneficial effects of the extract observed in vivo. Since CAW also improved mitochondrial function in the absence of Aβ, these results suggest a broader utility for other conditions where neuronal mitochondrial dysfunction occurs.

scholarly journals Protective effects of a cocktail of lactic acid bacteria on microcystin-LR-induced hepatotoxicity and oxidative damage in BALB/c mice

RSC Advances ◽  
2017 ◽  
Vol 7 (33) ◽  
pp. 20480-20487 ◽  
Author(s):  
Jichun Zhao ◽  
Fengwei Tian ◽  
Qixiao Zhai ◽  
Ruipeng Yu ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Oxidative Damage ◽  
Protective Effects ◽  
And Oxidative Stress

The aim of this study was to investigate the effects of mixed lactic acid bacteria (LAB) against microcystin-LR-exposed hepatotoxicity and oxidative stress in BALB/c mice.

scholarly journals Administration of Enalapril Started Late in Life Attenuates Hypertrophy and Oxidative Stress Burden, Increases Mitochondrial Mass, and Modulates Mitochondrial Quality Control Signaling in the Rat Heart

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 177 ◽  
Author(s):  
Anna Picca ◽  
Giuseppe Sirago ◽  
Vito Pesce ◽  
Angela Maria Serena Lezza ◽  
Riccardo Calvani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quality Control ◽  
Transcription Factor ◽  
Oxidative Damage ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Transcription ◽  
Mitochondrial Mass ◽  
Mitochondrial Transcription Factor ◽  
Mitochondrial Transcription Factor A ◽  
And Oxidative Stress

Mitochondrial dysfunction is a relevant mechanism in cardiac aging. Here, we investigated the effects of late-life enalapril administration at a non-antihypertensive dose on mitochondrial genomic stability, oxidative damage, and mitochondrial quality control (MQC) signaling in the hearts of aged rats. The protein expression of selected mediators (i.e., mitochondrial antioxidant enzymes, energy metabolism, mitochondrial biogenesis, dynamics, and autophagy) was measured in old rats randomly assigned to receive enalapril (n = 8) or placebo (n = 8) from 24 to 27 months of age. We also assessed mitochondrial DNA (mtDNA) content, citrate synthase activity, oxidative lesions to protein and mtDNA (i.e., carbonyls and the abundance of mtDNA4834 deletion), and the mitochondrial transcription factor A (TFAM) binding to specific mtDNA regions. Enalapril attenuated cardiac hypertrophy and oxidative stress-derived damage (mtDNA oxidation, mtDNA4834 deletion, and protein carbonylation), while increasing mitochondrial antioxidant defenses. The binding of mitochondrial transcription factor A to mtDNA regions involved in replication and deletion generation was enhanced following enalapril administration. Increased mitochondrial mass as well as mitochondriogenesis and autophagy signaling were found in enalapril-treated rats. Late-life enalapril administration mitigates age-dependent cardiac hypertrophy and oxidative damage, while increasing mitochondrial mass and modulating MQC signaling. Further analyses are needed to conclusively establish whether enalapril may offer cardioprotection during aging.

scholarly journals Self-Reported Exposure to ETS (Environmental Tobacco Smoke), Urinary Cotinine, and Oxidative Stress Parameters in Pregnant Women—The Pilot Study

2019 ◽  
Vol 16 (9) ◽  
pp. 1656 ◽  
Author(s):  
Lubica Argalasova ◽  
Ingrid Zitnanova ◽  
Diana Vondrova ◽  
Monika Dvorakova ◽  
Lucia Laubertova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Pregnant Women ◽  
Environmental Tobacco Smoke ◽  
Tobacco Smoke ◽  
Passive Smoking ◽  
Oxidative Stress Parameters ◽  
And Oxidative Stress ◽  
Stress Parameters

Background: Exposure to ETS (environmental tobacco smoke) is one of the most toxic environmental exposures. Objective: To investigate the association of ETS with physiological, biochemical, and psychological indicators, as well as with urine antioxidant capacity (AC) and oxidative damage to lipids in a pilot sample of healthy pregnant women. Methods: Exposure to ETS was investigated via a validated questionnaire, and urine cotinine and the marker of oxidative damage to lipids via 8-isoprostane concentrations using an ELISA kit. Urine AC was determined by the spectrophotometric Trolox-equivalent antioxidant capacity (TEAC) method. From a sample of pregnant women (n = 319, average age 30.84 ± 5.09 years) in 80, the levels of cotinine and oxidative stress markers were analyzed. Results: Among the 80 pregnant women, 5% (7.4% confirmed by cotinine) reported being current smokers and 25% reported passive smoking in the household (18.8% confirmed by cotinine). The Kappa was 0.78 for smokers and 0.22 for ETS-exposed nonsmokers. Pregnant women in the ETS-exposed group had significantly reduced AC compared to both the nonsmoker (ETS−) and the smoker groups (p < 0.05). Nonsmokers had significantly lower levels of 8-isoprostane than smokers (p < 0.01) and ETS-exposed nonsmokers (p < 0.05). Correlations between urine levels of cotinine and AC were positive in ETS-exposed nonsmokers. Conclusion: A harmful association of active and passive smoking and oxidative stress parameters among pregnant women has been indicated.

Quercetin protects rat hepatocytes from oxidative damage induced by ethanol and iron by maintaining intercellular liable iron pool

2013 ◽  
Vol 33 (5) ◽  
pp. 534-541 ◽  
Author(s):  
Y Li ◽  
Y Deng ◽  
Y Tang ◽  
H Yu ◽  
C Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Iron Overload ◽  
Combined Treatment ◽  
Rat Hepatocytes ◽  
Redox Status ◽  
Glutathione Depletion ◽  
Labile Iron Pool ◽  
Iron Pool ◽  
And Oxidative Stress

Accumulating evidence has shown that ethanol-induced iron overload plays a crucial role in the development and progression of alcoholic liver disease. We designed the present study to investigate the potential protective effect of quercetin, a naturally occurring iron-chelating antioxidant on alcoholic iron overload and oxidative stress. Ethanol-incubated (100 mmol/L) rat primary hepatocytes were co-treated by quercetin (100 µmol/L) and different dose of ferric nitrilotriacetate (Fe-NTA) for 24 h. When the hepatic enzyme releases in the culture medium, redox status of hepatocytes and the intercellular labile iron pool (LIP) level were assayed. Our data showed that Fe-NTA dose dependently induced cellular leakage of aspartate transaminase and lactate dehydrogenase, glutathione depletion, superoxide dismutase inactivation, and overproduction of malondialdehyde) and reactive oxygen species (ROS) of intact and especially ethanol-incubated hepatocytes. The oxidative damage resulted from ethanol, Fe-NTA, and especially their combined treatment was substantially alleviated by quercetin, accompanying the corresponding normalization of intercellular LIP level. Iron in excess, thus, may aggravate ethanol hepatotoxicity through Fenton-active LIP, and quercetin attenuated ethanol-induced iron and oxidative stress. To maintain intercellular LIP contributes to the hepatoprotective effect of quercetin besides its direct ROS-quenching activity.

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