Low-dose PCB126 exposure disrupts cardiac metabolism and causes hypertrophy and fibrosis in mice

Wang, Can; Cui, Ruina; Niu, Congying; Zhong, Xingwu; Zhu, Qicheng; Ji, Di; Li, Xianjie; Zhang, Hongxia; Liu, Chunqiao; Zhou, Lina; Li, Yanli; Xu, Guowang; Wei, Yanhong

doi:10.1016/j.envpol.2021.118079

Cited by 13 publications

(6 citation statements)

References 67 publications

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“…The contradiction between the results of our study and the study conducted by Wang et al (2021) may be due to the difference in the PCB congeners.…”

Section: Heart Organ Weightscontrasting

confidence: 99%

“…2021) found that low dose (0.5 µg/kg and 50 µg/kg) PCB126 exposure caused an increase in relative heart weights. This increase is thought to be related to cardiac hypertrophy seen with low-dose exposure [45]. In our study, we can suggest that the inhibition of heart tissue development due to oxidative damage caused by high-dose A1254 exposure may be the underlying factor of lower heart and relative heart weights in A1254-exposed groups.…”

Section: Heart Organ Weightsmentioning

confidence: 51%

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Toxic Effects of Aroclor 1254 on Rat Heart and Thyroid and Modifying Role of Selenium Status

Ozyurt

Özkemahlı

SUR

et al. 2023

Ankara Ecz. Fak. Derg.

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Objective: Polychlorinated biphenyls (PCBs) were very widely used in industrial products in past. These chemicals were banned in the 1970s due to their toxic effects. PCBs can still affect human health, as they are persistent in the environment. Aroclor 1254 (A1254) is a commercial PCB congener which was used in electrical transformers, fluorescent lighting fixtures and old appliances such as televisions or refrigerators. In this study, we aimed to evaluate the toxic effects of A1254 on heart and thyroid in male Sprague-Dawley rats. In addition, the modifying role of selenium status was also evaluated. Material and Method: 8-week-old male Sprague-Dawley (SD) rats were used in the experiment. The animals were separated randomly into 6 groups (n=6) as control; selenium supplemented (SeS); selenium deficient (SeD); A1254 exposed (A); selenium supplemented A1254 exposed (ASeS) and selenium deficient A1254 exposed (ASeD). A1254 was applied by gavage during the last 15 days of feeding period. Heart and thyroid weights and relative weights, plasma thyroid hormone levels, as well as thyroid and heart tissue oxidative/antioxidative parameters were evaluated. Result and Discussion: Results showed that A1254 exposure and selenium deficiency caused oxidative stress on both heart and thyroid. Plasma fT3 and fT4 levels markedly changed in ASeD group. In conclusion, it can be stated that A1254 exposure can cause lead to oxidative/antioxidative imbalance in both thyroid and heart and can disrupt functioning of thyroid hormones. Selenium seems to have a modifying role in A1254 toxicity in both organs, the importance of which should be evaluated with further mechanistic experiments.

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“…The contradiction between the results of our study and the study conducted by Wang et al (2021) may be due to the difference in the PCB congeners.…”

Section: Heart Organ Weightscontrasting

confidence: 99%

Section: Heart Organ Weightsmentioning

confidence: 51%

Toxic Effects of Aroclor 1254 on Rat Heart and Thyroid and Modifying Role of Selenium Status

Ozyurt

Özkemahlı

SUR

et al. 2023

Ankara Ecz. Fak. Derg.

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“…Ferroptosis and glutathione metabolism are essential for pathogen defense in the host, and the downregulation of their activities could disrupt intestinal homeostasis ( 75 , 76 ) and promote the invasion of E. piscicida . In addition, the TCA cycle, histidine metabolism, and taurine and hypotaurine metabolism were altered after E. piscicida infection, indicating disturbance in host energy metabolism ( 77 ) and immune defense mechanisms ( 78 , 79 ). Collectively, these results suggest that E. piscicida infection affects energy metabolism and disrupts the defense mechanisms of big-belly seahorses by inhibiting nutrient transport, signal transduction, and translation to promote virulence regulation, replication, and transmission.…”

Section: Discussionmentioning

confidence: 99%

Edwardsiella piscicida infection reshapes the intestinal microbiome and metabolome of big-belly seahorses: mechanistic insights of synergistic actions of virulence factors

et al. 2023

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Uncovering the mechanism underlying the pathogenesis of Edwardsiella piscicida-induced enteritis is essential for global aquaculture. In the present study, we identified E. piscicida as a lethal pathogen of the big-belly seahorse (Hippocampus abdominalis) and revealed its pathogenic pattern and characteristics by updating our established bacterial enteritis model and evaluation system. Conjoint analysis of metagenomic and metabolomic data showed that 15 core virulence factors could mutually coordinate the remodeling of intestinal microorganisms and host metabolism and induce enteritis in the big-belly seahorse. Specifically, the Flagella, Type IV pili, and Lap could significantly increase the activities of the representative functional pathways of both flagella assembly and bacterial chemotaxis in the intestinal microbiota (P < 0.01) to promote pathogen motility, adherence, and invasion. Legiobactin, IraAB, and Hpt could increase ABC transporter activity (P < 0.01) to compete for host nutrition and promote self-replication. Capsule1, HP-NAP, and FarAB could help the pathogen to avoid phagocytosis. Upon entering epithelial cells and phagocytes, Bsa T3SS and Dot/Icm could significantly increase bacterial secretion system activity (P < 0.01) to promote the intracellular survival and replication of the pathogen and the subsequent invasion of the neighboring tissues. Finally, LPS3 could significantly increase lipopolysaccharide biosynthesis (P < 0.01) to release toxins and kill the host. Throughout the pathogenic process, BopD, PhoP, and BfmRS significantly activated the two-component system (P < 0.01) to coordinate with other VFs to promote deep invasion. In addition, the levels of seven key metabolic biomarkers, Taurine, L-Proline, Uridine, L-Glutamate, Glutathione, Xanthosine, and L-Malic acid, significantly decreased (P < 0.01), and they can be used for characterizing E. piscicida infection. Overall, the present study systematically revealed how a combination of virulence factors mediate E. piscicida-induced enteritis in fish for the first time, providing a theoretical reference for preventing and controlling this disease in the aquaculture of seahorses and other fishes.

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“…Mice exposed to PCB126 have been shown to increase collagen synthesis enzymes, thereby increasing the proteins required for extracellular matrix and fibrosis. 48 PCBs and organochlorine pesticides are capable of reducing paraoxonase (PON1), the lipophilic antioxidant factor of high-density lipoprotein (HDL) cholesterol. Increased POPs concentrations in HDL in CVD patients is accompanied by decreased PON1 activity which may impair HDL function to reduce LDL susceptibility to lipid peroxidation.…”

Section: Molecular Mechanism Of Toxicity Of Organochlorines Pesticide...mentioning

confidence: 99%

“… 46 Exposure to low-dose PCB126 disrupts cardiac energy metabolism by altering the regulatory function of the peroxisome proliferator-activated γ receptor (PPARγ) gene. 47 , 48 PPARs increase insulin sensitivity, mitochondrial function and the metabolism of fatty acids and glucose, as well as exert anti-inflammatory and anti-atherogenic properties on vascular walls and immune cells. 15 During heart failure, the mechanism of ATP production changes with the increasing rate of glucose uptake and glycolysis resulting in cardiac hypertrophy and myocardial fibrosis.…”

Section: Molecular Mechanism Of Toxicity Of Organochlorines Pesticide...mentioning

confidence: 99%

Insights into Organochlorine Pesticides Exposure in the Development of Cardiovascular Diseases: A Systematic Review

Mohammadkhani,

Shahrzad,

Haghighi

et al. 2023

Arch Iran Med

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Many human diseases such as cancer, neurological diseases, autism and diabetes are associated with exposure to pesticides, especially organochlorine pesticides. However, pesticide exposure is also associated with cardiovascular disease (CVD) as the leading cause of death worldwide. In this systematic review, results on the link between organochlorine pesticide pollution and CVD were collected from databases (Medline (PubMed), Scopus and Science Direct) in May 2022 from studies published between 2010 and 2022. A total of 24 articles were selected for this systematic review. Sixteen articles were extracted by reviewers using a standardized form that included cross-sectional, cohort, and ecological studies that reported exposure to organochlorine pesticides in association with increased CVD risk. In addition, eight articles covering molecular mechanisms organochlorine pesticides and polychlorinated biphenyls (PCBs) on cardiovascular effects were retrieved for detailed evaluation. Based on the findings of the study, it seems elevated circulating levels of organochlorine pesticides and PCBs increase the risk of coronary heart disease, especially in early life exposure to these pesticides and especially in men. Changes in the regulatory function of peroxisome proliferator-activated γ receptor (PPARγ), reduction of paroxonase activity (PON1), epigenetic changes of histone through induction of reactive oxygen species, vascular endothelial inflammation with miR-expression 126 and miR-31, increased collagen synthesis enzymes in the extracellular matrix and left ventricular hypertrophy (LVH) and fibrosis are mechanisms by which PCBs increase the risk of CVD. According to this systematic review, organochlorine pesticide exposure is associated with increased risk of CVD and CVD mortality through the atherogenic and inflammatory molecular mechanism involving fatty acid and glucose metabolism.

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Low-dose PCB126 exposure disrupts cardiac metabolism and causes hypertrophy and fibrosis in mice

Cited by 13 publications

References 67 publications

Toxic Effects of Aroclor 1254 on Rat Heart and Thyroid and Modifying Role of Selenium Status

Toxic Effects of Aroclor 1254 on Rat Heart and Thyroid and Modifying Role of Selenium Status

Edwardsiella piscicida infection reshapes the intestinal microbiome and metabolome of big-belly seahorses: mechanistic insights of synergistic actions of virulence factors

Insights into Organochlorine Pesticides Exposure in the Development of Cardiovascular Diseases: A Systematic Review

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