Cadmium induced skeletal underdevelopment, liver cell apoptosis and hepatic energy metabolism disorder in Bufo gargarizans larvae by disrupting thyroid hormone signaling

Ya, Jing; Xu, Yifan; Wang, Gang; Zhao, Hongfeng

doi:10.1016/j.ecoenv.2021.111957

Cited by 13 publications

(5 citation statements)

References 63 publications

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“…[36][37][38] Previous research works have shown a harmful influence on liver caused by Cd which can induce oxidative stress to relevant cells. [4,39,40] While, the liver plays a central role in whole-body lipid metabolism involving governing the synthesis, oxidization, transport, and excretion of lipids. Furthermore, the liver is the main organ for TG and LDL-C synthesis.…”

Section: Discussionmentioning

confidence: 99%

Cadmium influence on lipid metabolism in Sprague–Dawley rats through linoleic acid and glycerophospholipid metabolism pathways

Dong

Zhao

Yin

et al. 2023

J Biochem & Molecular Tox

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Cadmium (Cd) is widely distributed in the environment and easy adsorbed by living organisms with adverse effects. Exposure to Cd‐contaminated food may disrupt lipid metabolism and increase human health risk. To study the perturbation effect of Cd on lipid metabolism in vivo, 24 male Sprague–Dawley (SD) rats were randomly assigned four groups and treated by Cd chloride solution (0, 1.375 mg/kg, 5.5 mg/kg, 22 mg/kg) for 14 days. The characteristic indexes of serum lipid metabolism were analyzed. Afterwards, untargeted metabolomics analysis was applied to explore the adverse effects of Cd on rats by liquid chromatography coupled with mass spectrometry (LC‐MS). The results revealed that Cd exposure obviously decreased the average serum of triglycerides (TG) and low‐density lipoprotein cholesterol (LDL‐C) and caused an imbalance of endogenous compounds in the 22 mg/kg Cd‐exposed group. Compared with the control group, 30 metabolites with significant differences were identified in the serum. Our results indicated that Cd caused lipid metabolic disorders in rats by disrupting linoleic acid and glycerophospholipid metabolism pathways. Furthermore, there were three kinds of remarkable differential metabolites—9Z,12Z‐octadecadienoic acid, PC(20:4(8Z,11Z,14Z,17Z)/0:0), and PC(15:0/18:2(9Z,12Z)), which enriched the two significant metabolism pathways and could be the potential biomarkers.

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Section: Discussionmentioning

confidence: 99%

Cadmium influence on lipid metabolism in Sprague–Dawley rats through linoleic acid and glycerophospholipid metabolism pathways

Dong

Zhao

Yin

et al. 2023

J Biochem & Molecular Tox

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“…Previous studies demonstrated that Cd exposure in animals is associated with the trend of hypothyroxinemia [ 14 , 18 ]. Meanwhile, investigations in lower vertebrates reported that higher Cd could induce thyroid structural injuries and thyroid signaling disruption of bufo gargarizans and these studies indicated that high-dose Cd cause other adverse outcomes by disrupting the thyroid system [ 13 , 44 ]. Furthermore, the mechanism of Cd-induced thyrotoxicity was regarded as the consequence of Cd effects on pituitary secretion in some in vivo studies on rats [ 45 – 47 ].…”

Section: Discussionmentioning

confidence: 99%

Higher cadmium exposure was associated with sex-specific thyroid dysfunction: Consistent evidence from two independent cross-sectional studies based on urinary and blood cadmium measurements

Shao,

Su,

Wang

et al. 2023

Preprint

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Population-based studies on the association between cadmium (Cd) exposure and thyroid function are limited and have shown conflicting results. Two independent cross-sectional studies using different Cd biomarkers were carried out in six rural areas with different soil Cd levels in China. Thyroid dysfunction was defined based on levels of thyroid stimulating hormone (TSH) and free thyroxine (FT4). Both multivariable linear regression, multiple logistic regression and restrictive cubic splines models were used to estimate the association between Cd and thyroid dysfunction. For both of the two independent studies, higher Cd levels were observed to be associated with lower TSH levels and higher risk of thyroid dysfunction. The negative relationship between urinary Cd and TSH was found in both total participants (β = -0.072, p = 0.008) and males (β = -0.119, p = 0.020) but not in females, however, the negative relationship between blood Cd and TSH was only found in females (β = -0.104, p = 0.024). Higher urinary Cd (> 2.52 µg/g creatinine) was associated with higher risk of thyroid dysfunction, while higher blood Cd was associated with higher risk of hyperthyroidism status. The adjusted Odds Ratio (OR) for the risk of hyperthyroidism status was 3.48 (95%CI:1.36–8.92) and 6.94 (95%CI:1.23–39.31) times higher with every natural log unit higher in blood Cd in total participants and males, respectively. Results from the two independent cross-sectional studies consistently suggested that higher Cd levels were associated with sex-specific thyroid dysfunction.

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“…This has been demonstrated in cell models exposed to copper. [62][63][64] As mitochondria ultimately regulate metabolic activity and utilize fuel sources to generate ATP, 65 we assessed mitochondrial bioenergetics as an indicator of energy status. Based on the data presented here, basal OCR (F = 75.42, p < 0.0001), oligomycin-induced ATP production (F = 42.45, p < 0.0001), maximal OCR (F = 57.64, p < 0.0001) and spare capacity (F = 8.267, p = 0.0028) of cells were significantly decreased after exposure to 10 and 25 μg mL −1 copper concentrations of the nanopesticide and ions (Fig.…”

Section: Mitochondrial Bioenergetics and Oxidative Stress Responsesmentioning

confidence: 99%

“…As normal mitochondrial respiration is critical for cell survival, redox homeostasis, and nutrition utilization, 33,65,68,69 we conducted absolute quantitative metabolomic analysis of metabolites specifically involved in oxidative respiration. The energy-relevant metabolites and their corresponding energy pathways are listed in Table S2, † including 32 metabolites in glycolysis, tricarboxylic acid (TCA) cycle, OXPHOS and the pentose phosphate pathway.…”

Section: Targeted Metabolomic Analysis Of Energy-relevant Metabolitesmentioning

confidence: 99%

“…The rate of the TCA cycle is precisely adjusted to meet the energy needs of cells for ATP. 65,81 The primary control points are the allosteric enzymes, including IDH and α-KGDH. Decreased expression of key enzymes of the TCA cycle have been demonstrated to result in the accumulation of TCA cycle metabolites in RAW264.7 cells, Het-1A cells, Wistar rats and fish gills (Cyprinus carpio).…”

Section: Mitochondrial Functions: Tricarboxylic Acid Cyclementioning

confidence: 99%

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Metabolomic and bioenergetic responses of human hepatocellular carcinoma cells following exposure to commercial copper hydroxide nanopesticide

Li¹,

Qin²,

Kong³

et al. 2022

Environ. Sci.: Nano

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Cadmium induced skeletal underdevelopment, liver cell apoptosis and hepatic energy metabolism disorder in Bufo gargarizans larvae by disrupting thyroid hormone signaling

Cited by 13 publications

References 63 publications

Cadmium influence on lipid metabolism in Sprague–Dawley rats through linoleic acid and glycerophospholipid metabolism pathways

Cadmium influence on lipid metabolism in Sprague–Dawley rats through linoleic acid and glycerophospholipid metabolism pathways

Higher cadmium exposure was associated with sex-specific thyroid dysfunction: Consistent evidence from two independent cross-sectional studies based on urinary and blood cadmium measurements

Metabolomic and bioenergetic responses of human hepatocellular carcinoma cells following exposure to commercial copper hydroxide nanopesticide

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