Mitochondrial energy metabolism in the hepatopancreas of freshwater crabs (Sinopotamon henanense) after cadmium exposure

Yang, Jian; Li, Dongmei; He, Yongmei; Wang, Lan

doi:10.1039/c4em00453a

Cited by 23 publications

(16 citation statements)

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“…These experiments show that mitochondria respond to acute Cd exposure with an upregulation of energy production (higher levels of ΔΨ m , NADH/NAD+ and ATP/ADP ratio) to cope with the energy demand of cellular defense mechanisms such as metallothionein (MT) production. However, with increasing exposure time a decline of energy production accompanied by excessive mitochondrial impairment was observed [ 83 ]. Consequently, it can be stated that mitochondrial energetic homeostasis is a fundamental requirement for successful Cd defense [ 83 , 84 ] but long-term countermeasures may depend on a balanced mitochondrial turnover with the risk of emphasizing anti-apoptotic signaling.…”

Section: Resultsmentioning

confidence: 99%

“…However, with increasing exposure time a decline of energy production accompanied by excessive mitochondrial impairment was observed [ 83 ]. Consequently, it can be stated that mitochondrial energetic homeostasis is a fundamental requirement for successful Cd defense [ 83 , 84 ] but long-term countermeasures may depend on a balanced mitochondrial turnover with the risk of emphasizing anti-apoptotic signaling.…”

Section: Resultsmentioning

confidence: 99%

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Cadmium Protection Strategies—A Hidden Trade-Off?

Sandbichler

Höckner

2016

IJMS

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Cadmium (Cd) is a non-essential transition metal which is introduced into the biosphere by various anthropogenic activities. Environmental pollution with Cd poses a major health risk and Cd toxicity has been extensively researched over the past decades. This review aims at changing the perspective by discussing protection mechanisms available to counteract a Cd insult. Antioxidants, induction of antioxidant enzymes, and complexation of Cd to glutathione (GSH) and metallothionein (MT) are the most potent protective measures to cope with Cd-induced oxidative stress. Furthermore, protection mechanisms include prevention of endoplasmic reticulum (ER) stress, mitophagy and metabolic stress, as well as expression of chaperones. Pre-exposure to Cd itself, or co-exposure to other metals or trace elements can improve viability under Cd exposure and cells have means to reduce Cd uptake and improve Cd removal. Finally, environmental factors have negative or positive effects on Cd toxicity. Most protection mechanisms aim at preventing cellular damage. However, this might not be possible without trade-offs like an increased risk of carcinogenesis.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Cadmium Protection Strategies—A Hidden Trade-Off?

Sandbichler

Höckner

2016

IJMS

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“…Cadmium (Cd) is a serious environmental pollutant which occurs naturally, it could be released into environments by natural processes and human activities [1]. There exists certain amounts of Cd in different rivers and sea waters [2, 3].…”

Section: Introductionmentioning

confidence: 99%

“…Cd has been classified as a cumulative toxicant, with its biological half-life of over 10–30 years [5]. Therefore, the ecological risk of waterborne Cd is of particular concern on account of its toxicity toward aquatic organisms, including fish [6], freshwater mussels [7] as well as crabs [1, 5, 8–14].…”

Section: Introductionmentioning

confidence: 99%

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Identification and profiling of microRNAs responsive to cadmium toxicity in hepatopancreas of the freshwater crab Sinopotamon henanense

Guo

Xie

et al. 2019

Hereditas

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BackgroundCadmium (Cd) is a ubiquitous environmental toxicant for aquatic animals. The freshwater crab, Sinopotamon henanense (S. henanense), is a useful model for monitoring Cd exposure since it is widely distributed in sediments whereby it tends to accumulate several toxicants, including Cd. In the recent years, the toxic effects of Cd in the hepatopancreas of S. henanense have been demonstrated by a series of biochemical analysis and ultrastructural observations as well as the deep sequencing approaches and gene expression profile analysis. However, the post-transcriptional regulatory network underlying Cd toxicity in S.henanense is still largely unknown.ResultsThe miRNA transcriptional profile of the hepatopancreas of S. henanense was used to investigate the expression levels of miRNAs in response to Cd toxicity. In total, 464 known miRNAs and 191 novel miRNAs were identified. Among these 656 miRNAs, 126 known miRNAs could be matched with the miRNAs of Portunus trituberculatus, Eriocheir sinensis and Scylla paramamosain. Furthermore, a total of 24 conserved miRNAs were detected in these four crab species. Fifty-one differentially expressed miRNAs were identified in the Cd-exposed group, with 31 up-regulated and 20 down-regulated. Eight of the differentially expressed miRNAs were randomly selected and verified by the quantitative real-time PCR (qRT-PCR), and there was a general consistency (87.25%) between the qRT-PCR and miRNA transcriptome data. A total of 5258 target genes were screened by bioinformatics prediction. GO term analysis showed that, 17 GO terms were significantly enriched, which were mainly related to the regulation of oxidoreductase activity. KEGG pathway analysis showed that 18 pathways were significantly enriched, which were mainly associated with the biosynthesis, modification and degradation of proteins.ConclusionIn response to Cd toxicity, in the hepatopancreas of S. henanense, the expressions of significant amount of miRNAs were altered, which may be an adaptation to resist the oxidative stress induced by Cd. These results provide a basis for further studies of miRNA-mediated functional adaptation of the animal to combat Cd toxicity.

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Bioenergetics‐adverse outcome pathway: Linking organismal and suborganismal energetic endpoints to adverse outcomes

Goodchild

Simpson

Minghetti

et al. 2018

Enviro Toxic and Chemistry

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Adverse outcome pathways (AOPs) link toxicity across levels of biological organization, and thereby facilitate the development of suborganismal responses predictive of whole‐organism toxicity and provide the mechanistic information necessary for science‐based extrapolation to population‐level effects. Thus far AOPs have characterized various acute and chronic toxicity pathways; however, the potential for AOPs to explicitly characterize indirect, energy‐mediated effects from toxicants has yet to be fully explored. Indeed, although exposure to contaminants can alter an organism's energy budget, energetic endpoints are rarely incorporated into ecological risk assessment because there is not an integrative framework for linking energetic effects to organismal endpoints relevant to risk assessment (e.g., survival, reproduction, growth). In the present analysis, we developed a generalized bioenergetics‐AOP in an effort to make better use of energetic endpoints in risk assessment, specifically exposure scenarios that generate an energetic burden to organisms. To evaluate empirical support for a bioenergetics‐AOP, we analyzed published data for links between energetic endpoints across levels of biological organization. We found correlations between 1) cellular energy allocation and whole‐animal growth, and 2) metabolic rate and scope for growth. Moreover, we reviewed literature linking energy availability to nontraditional toxicological endpoints (e.g., locomotor performance), and found evidence that toxicants impair aerobic performance and activity. We conclude by highlighting current knowledge gaps that should be addressed to develop specific bioenergetics‐AOPs. Environ Toxicol Chem 2019;38:27–45. © 2018 SETAC

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Mitochondrial energy metabolism in the hepatopancreas of freshwater crabs (Sinopotamon henanense) after cadmium exposure

Abstract: Following Cd exposure, volume expansion and swollen matrices in more mitochondria could lead to disturbance in mitochondrial morphology.

Cited by 23 publications

References 45 publications

Cadmium Protection Strategies—A Hidden Trade-Off?

Cadmium Protection Strategies—A Hidden Trade-Off?

Identification and profiling of microRNAs responsive to cadmium toxicity in hepatopancreas of the freshwater crab Sinopotamon henanense

Bioenergetics‐adverse outcome pathway: Linking organismal and suborganismal energetic endpoints to adverse outcomes

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