Chlorinated herbicides in fish, birds and mammals in the Baltic Sea

Reindl, Andrzej R.; Falkowska, Lucyna; Grajewska, Agnieszka

doi:10.1007/s11270-015-2536-x

Cited by 30 publications

(16 citation statements)

References 34 publications

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“…We also found pathways in the core metabolism that are involved in the degradation of persistent pollutants and plastics such as atrazine [65], bisphenol [66], and chlorobenzene [67] (S6 Table). The accumulation of harmful substances has been reported in the tissues of marine mammals [68], with the degradation of these toxic compounds mainly depending on the metabolism of bacteria.…”

Section: Resultsmentioning

confidence: 99%

The Pacific harbor seal gut microbiota in Mexico: Its relationship with diet and functional inferences

et al. 2019

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Diet is a primary driver of the composition of gut microbiota and is considered one of the main routes of microbial colonization. Prey identification is fundamental for correlating the diet with the presence of particular microbial groups. The present study examined how diet influenced the composition and function of the gut microbiota of the Pacific harbor seal ( Phoca vitulina richardii ) in order to better understand the role of prey consumption in shaping its microbiota. This species is a good indicator of the quality of the local environment due to both its foraging and haul-out site fidelity. DNA was extracted from 20 fecal samples collected from five harbor seal colonies located in Baja California, Mexico. The V4 region of 16S rRNA gene was amplified and sequenced using the Illumina technology. Results showed that the gut microbiota of the harbor seals was dominated by the phyla Firmicutes (37%), Bacteroidetes (26%) and Fusobacteria (26%) and revealed significant differences in its composition among the colonies. Funtional analysis using the PICRUSt software suggests a high number of pathways involved in the basal metabolism, such as those for carbohydrates (22%) and amino acids (20%), and those related to the degradation of persistent environmental pollutants. In addition, a DNA metabarcoding analysis of the same samples, via the amplification and sequencing of the mtRNA 16S and rRNA 18S genes, was used to identify the prey consumed by harbor seals revealing the consumption of prey with mainly demersal habits. Functional redundancy in the seal gut microbiota was observed, irrespective of diet or location. Our results indicate that the frequency of occurrence of specific prey in the harbor seal diet plays an important role in shaping the composition of the gut microbiota of harbor seals by influencing the relative abundance of specific groups of gut microorganisms. A significant relationship was found among diet, gut microbiota composition and OTUs assigned to a particular metabolic pathway.

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Section: Resultsmentioning

confidence: 99%

The Pacific harbor seal gut microbiota in Mexico: Its relationship with diet and functional inferences

et al. 2019

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“…Liver is an essential organ involved in the metabolism of exogenous toxic substance and also a primary target of ATR toxicity. It is known to cause hepatic damage in frogs, fish, birds, pigs, and rodents . The use of histologic and ultrastructural analysis allowed for the damage of target organelle in the microsomes by exposure to ATR .…”

Section: Discussionmentioning

confidence: 99%

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

Qin

Lin

et al. 2017

Environmental Toxicology

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Atrazine (ATR) is one of the most widely detected contaminant in the ecosystem. Nuclear xenobiotic receptors are activated by herbicides and induce the transcription of CYP450 isoforms involved in xenobiotic metabolism and transport. However, little is known about hepatic nuclear xenobiotic receptors in birds are responsible for ATR-induced hepatotoxicity via regulating the cytochrome P450 enzyme systems (CYP450s). The objective of this study was to investigate the mechanism of ATR hepatotoxicity in quails. For this purpose, male quails were dosed by oral gavage from sexual immaturity to maturity with 0, 50, 250, and 500 mg/kg/day ATR for 45 days. The results showed that ATR exposure caused the hepatotoxicity damage and endoplasmic reticulum (ER) degeneration. It suggested that ER is a target organelle of ATR toxicity in hepatocytes. ATR exposure disrupted the hepatic CYP450s homeostasis. This study also demonstrated that ATR triggered the CYP450 isoforms transcription via activating the hepatic CAR/PXR pathway. The present study provides new insights regarding the mechanism of the ATR-induced hepatotoxicity through activating nuclear xenobiotic receptors and triggering ER stress and hepatic CYP450s in quails.

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“…According to previous studies, atrazine can induce pathological effects in multiple tissues [ 7 , 12 ]. Atrazine was recorded in the liver and heart [ 46 - 49 ], suggesting the heart and liver are organs involved in the metabolism of atrazine. Our previous study showed that atrazine induced significantly ionic disorder in the liver and heart on mice as well [ 18 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases

Lin

Qin

et al. 2016

Oncotarget

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The widely used atrazine has been reported to exhibit extensive ecological hazards. Due to the biological accumulation, atrazine elicits widespread toxic effects on different organisms. However, true proof for the mechanism of atrazine-induced toxicity is lacking. To determine the potential mechanism by which atrazine exerted toxic effects, quails were treated with atrazine (0, 50, 250 and 500 mg/kg) by gavage administration for 45 days. Atrazine significantly increased the histological alterations and serum creatine kinase, lactate dehydrogenase and choline esterase levels. A marked disorder in ionic (Na+, K+, Ca2+ and Mg2+)contents and the decrease of ATPases (Na+-K+-ATPase, Ca2+-ATPase, Mg2+-ATPase and Ca2+-Mg2+-ATPase) activities were observed in the heart and liver of atrazine-exposed quails. Of note, it was also observed that atrazine suppressed the transcription of Na+, K+ transfer associated genes (Na+-K+-ATPase subunits) and Ca2+ transfer associated genes (Ca2+-ATPase subunits, solute carriers) in heart and liver. In conclusion, atrazine induced cardiac and hepatic damage via causing the ionic disorder, triggering the transcription of the ion transporters and leading the histopathological and functional alternations in the heart and liver of quails. This study demonstrated atrazine significantly induced the ionic disorder via decreasing the ATPases activities and disturbing the transcription of the ion transporters.

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Chlorinated herbicides in fish, birds and mammals in the Baltic Sea

Cited by 30 publications

References 34 publications

The Pacific harbor seal gut microbiota in Mexico: Its relationship with diet and functional inferences

The Pacific harbor seal gut microbiota in Mexico: Its relationship with diet and functional inferences

Activating nuclear xenobiotic receptors and triggering ER stress and hepatic cytochromes P450 systems in quails (Coturnix C. coturnix) during atrazine exposure

A novel mechanism underlies atrazine toxicity in quails (Coturnix Coturnix coturnix): triggering ionic disorder via disruption of ATPases

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