Changes on serum and hepatic lipidome after a chronic cadmium exposure in Wistar rats

Sarmiento-Ortega, Víctor Enrique; Treviño, Samuel; Flores‐Hernández, Jorge; Aguilar-Alonso, Patrícia; Moroni-González, Diana; Aburto-Luna, Violeta; Díaz, Alfonso López; Brambila, Eduardo

doi:10.1016/j.abb.2017.10.003

Cited by 30 publications

(18 citation statements)

References 73 publications

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“…Further to this, another study using rats focused on the effects of excess Cd. Upon exposure to excess Cd, an increase was observed in hepatic cholesterol, phospholipids, and triglycerides ( Sarmiento-Ortega et al, 2017 ). These studies suggest a close connection between the metallome and lipidome.…”

Section: Introductionmentioning

confidence: 99%

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Stanton

Malijauskaite

McGourty

et al. 2021

Front. Mol. Neurosci.

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Metal dyshomeostasis plays a significant role in various neurological diseases such as Alzheimer’s disease, Parkinson’s disease, Autism Spectrum Disorders (ASD), and many more. Like studies investigating the proteome, transcriptome, epigenome, microbiome, etc., for years, metallomics studies have focused on data from their domain, i.e., trace metal composition, only. Still, few have considered the links between other “omes,” which may together result in an individual’s specific pathologies. In particular, ASD have been reported to have multitudes of possible causal effects. Metallomics data focusing on metal deficiencies and dyshomeostasis can be linked to functions of metalloenzymes, metal transporters, and transcription factors, thus affecting the proteome and transcriptome. Furthermore, recent studies in ASD have emphasized the gut-brain axis, with alterations in the microbiome being linked to changes in the metabolome and inflammatory processes. However, the microbiome and other “omes” are heavily influenced by the metallome. Thus, here, we will summarize the known implications of a changed metallome for other “omes” in the body in the context of “omics” studies in ASD. We will highlight possible connections and propose a model that may explain the so far independently reported pathologies in ASD.

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Section: Introductionmentioning

confidence: 99%

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Stanton

Malijauskaite

McGourty

et al. 2021

Front. Mol. Neurosci.

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“…This is the reason for selecting the LOAEL dose (32.5 ppm), as it is the known dose that increases circulating Cd levels over time, according to the report by Agency for toxic substances and disease registry‐CDC and (Treviño et al, 2015b). Each group was subdivided into three ( n = 12) to evaluate the Cd exposure effect by 2, 3, and 4 months (Sarmiento‐Ortega et al, 2017; Pulido et al, 2019).…”

Section: Methodsmentioning

confidence: 99%

“…Reports indicate that Cd LOAEL dose generates structural and functional damage in the liver, kidney, pancreas, testes, and ovaries (Wang et al, 2021). Since gastrointestinal Cd absorption is around 10% of the total content in food and water, the LOAEL 32.5 ppm of Cd represent an environmental exposure, which we reported that generates metabolic disruption such as insulin resistance in the liver, muscle, adipose, and cardiovascular tissues, and induces hyperglycemia and dyslipidemia (Sarmiento‐Ortega et al, 2017; Treviño et al, 2015b). In humans, chronic Cd LOAEL exposure has renal effects demonstrated by elevated concentration in urine of proteins, albumin, N‐acetyl‐β‐D‐glucosaminidase, β2‐microglobulin, and cadmium (Satarug et al., 2017; Satarug, 2018).…”

Section: Introductionmentioning

confidence: 96%

Effect of cadmium administration on the antioxidant system and neuronal death in the hippocampus of rats

Treviño

Pulido

Fuentes

et al. 2022

Synapse

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Cadmium (Cd) is a heavy metal classified as a carcinogen whose exposure could affect the function of the central nervous system. Studies suggest that Cd modifies neuronal morphology in the hippocampus and affects cognitive tasks. The oxidative stress pathway is proposed as a mechanism of toxicity. However, this mechanism is not precise yet. This study aimed to evaluate the effect of Cd administration on oxidative stress markers in the male rat's hippocampus. Male Wistar rats were divided into (1) control (drinking water) and (2) treatment with Cd (32.5 ppm of cadmium chloride (CdCl2) in water). The Cd was administered for 2, 3, and 4 months. The results show that the oral administration of CdCl2 increased the concentration of Cd in plasma and hippocampus, and this response is time‐dependent on its administration. Likewise, it caused an increase in lipid peroxidation and nitrosative stress markers. Moreover, it increased reactive astrogliosis and antioxidant enzyme activity. Consequently, the progression of the oxidative response exacerbated neurodegeneration in hippocampal cells. Our results suggest that Cd exposure induces a severe oxidative response that contributes critically to hippocampal neurodegeneration. It is suggested that exposure to Cd increases the risk of developing neurological diseases, which contributes to a decrease in the quality of life of the human and the environment in which it lives.

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“…However, it is unrelated to the death of β-cells [ 75 ]. Chronic-Cd exposure in drinking water elicits changes in insulin secretion and insulin resistance development [ 76 , 77 ]. Progressive hyperinsulinemia is an adaptive response by β-cells.…”

Section: Cadmium and Pancreatic β-Cellsmentioning

confidence: 99%

Pancreas–Liver–Adipose Axis: Target of Environmental Cadmium Exposure Linked to Metabolic Diseases

Moroni-González

Sarmiento-Ortega

Díaz

et al. 2023

Toxics

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Cadmium has been well recognized as a critical toxic agent in acute and chronic poisoning cases in occupational and nonoccupational settings and environmental exposure situations. Cadmium is released into the environment after natural and anthropogenic activities, particularly in contaminated and industrial areas, causing food pollution. In the body, cadmium has no biological activity, but it accumulates primarily in the liver and kidney, which are considered the main targets of its toxicity, through oxidative stress and inflammation. However, in the last few years, this metal has been linked to metabolic diseases. The pancreas–liver–adipose axis is largely affected by cadmium accumulation. Therefore, this review aims to collect bibliographic information that establishes the basis for understanding the molecular and cellular mechanisms linked to cadmium with carbohydrate, lipids, and endocrine impairments that contribute to developing insulin resistance, metabolic syndrome, prediabetes, and diabetes.

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Changes on serum and hepatic lipidome after a chronic cadmium exposure in Wistar rats

Cited by 30 publications

References 73 publications

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

The Metallome as a Link Between the “Omes” in Autism Spectrum Disorders

Effect of cadmium administration on the antioxidant system and neuronal death in the hippocampus of rats

Pancreas–Liver–Adipose Axis: Target of Environmental Cadmium Exposure Linked to Metabolic Diseases

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