Gut as a target for cadmium toxicity

Tinkov, Alexey A.; Гриценко, В. А.; Skalnaya, Margarita G.; Черкасов, С. В.; Aaseth, Jan; Skalny, Anatoly V.

doi:10.1016/j.envpol.2017.12.114

Cited by 187 publications

(73 citation statements)

References 66 publications

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“…Recently, it has been estimated that dietary Cd exposure contributed to 0.2% of the global burden of chronic kidney disease [9]. Apart from the primary stores, Cd-induced damage has also been reported in brain [10], cardiovascular system [11] [12], nervous system [13], immune system [14], gut [15] and reproductive system [16] [17]. In addition to its ability to bioaccumulate, a relatively small fraction (0.007%) of Cd is excreted from the body as urine and feces [4].…”

Section: Cadmium As An Environmental Pollutantmentioning

confidence: 99%

Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Das¹,

Al‐Naemi²

2019

ODEM

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Cadmium is a known environmental pollutant targeting various organs. Often implicated in cadmium toxicology is the formation of reactive oxygen species, overwhelming the free radical scavenging mechanisms and inducing oxidative stress. Acute cadmium intoxication has been shown to reduce antioxidant enzyme activity and induce oxidative stress. However, chronic intoxication has obscure outcomes in oxidative stress while the cell makes adjustments to overcome the toxicant load. Also linked with the occurrence of oxidative stress is inflammation. Stimulation of acute or chronic inflammation is mediated by different cascades. However, key events include activation of transcription factor, NF-κB and release of pro-inflammatory cytokines. Both oxidative stress and inflammation are implicated simultaneously in pathogenesis and induction of multi-organ tissue damage under cadmium exposure. This article reviews the impact of acute and chronic cadmium intoxication on inducing oxidative stress, inflammation and thereby inflicting tissue damage.

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Section: Cadmium As An Environmental Pollutantmentioning

confidence: 99%

Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Das¹,

Al‐Naemi²

2019

ODEM

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“…Tobacco smoking is a major source of Cd intake, a cigarette contains 5 mg of this metal, which could lead to significantly 4–5 times higher levels of Cd in smokers’ blood than that of non‐smokers (Djuric et al, 2015; Takiguchi & Yoshihara, 2006). Generally, the Cd poisoning is the result of a chronic exposure, which is mainly reflected to bone (Järup, Alfvén, Persson, Toss and Elinder, 1998; Knani, Bartolini, et al, 2019; Knani, Venditti, et al, 2019; Xie & Sheng, 2017), kidney (Johri, Jacquillet, & Unwin, 2010; Satarug, 2018), gastrointestinal tract (Tinkov et al, 2018), lung (Ganguly, Levänen, Palmberg, Åkesson, & Lindén, 2018), and testis pathologies, whereas the latest one is the major target organ of Cd toxicity, due to its high sensitivity (Siu, Mruk, Porto, & Cheng, 2009).…”

Section: Introductionmentioning

confidence: 99%

Cadmium‐induced toxicity increases prolyl endopeptidase (PREP) expression in the rat testis

Venditti

Chemek²,

Minucci

et al. 2020

Molecular Reproduction Devel

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During the differentiation of the male gamete, there is a massive remodeling in the shape and architecture of all the cells of the seminiferous epithelium. The cytoskeleton, as well as many associated proteins with it, plays a pivotal role in this process. The testis is particularly susceptible to environmental pollutant, which can lead to injury and impairment of normal spermatozoa production. Cadmium (Cd) is one of the major chemical environmental toxicants in economically developed countries. Food and cigarettes are the main sources of exposure to this element.Here, the protective role of zinc (Zn) to prevent the testicular toxicity in male adult rats after prenatal and during lactation exposure to Cd has been assessed. Altered testicular histology at the interstitial and germinal levels was found, whereas Zn supply completely corrected Cd toxicity. Moreover, the effects of these metals on the testicular expression and localization of the protease prolyl endopeptidase (PREP) were evaluated. Interestingly, the results showed an increase of PREP messenger RNA and protein. Data were corroborated by immunofluorescence. This study raises the possibility of using PREP as a new fertility marker. K E Y W O R D Scadmium, endocrine disruptor, PREP, testis, zinc

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“…Metabolites of arsenic alter gut bacterial species, the production of butyrate, and the gut-associated immune system [34]. Cadmium exposure determines an inflammatory response and tight junction alterations in the intestinal barrier that increase gut permeability and favour the Bacteroidetes in the microbiome [35]. Antibiotics, nanoparticles as environmental pollution, and additives used for food preservation influence and alter the composition and function of the gut microbiota, predisposing to the onset of diseases [36].…”

Section: Environmental Factors Environmental Influences Alonementioning

confidence: 99%

Molecular Aspects of Colorectal Adenomas: The Interplay among Microenvironment, Oxidative Stress, and Predisposition

Aceto

Catalano

Curia

2020

BioMed Research International

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The development of colorectal cancer (CRC) is a multistep process initiated by a benign polyp that has the potential to evolve into in situ carcinoma through the interactions between environmental and genetic factors. CRC incidence rates are constantly increased for young adult patients presenting an advanced tumor stage. The majority of CRCs arise from colonic adenomas originating from aberrant cell proliferation of colon epithelium. Endoscopic polypectomy represents a tool for early detection and removal of polyps, although the occurrence of cancers after negative colonoscopy shows a significant incidence. It has long been recognized that the aberrant regulation of Wingless/It (Wnt)/β-Catenin signaling in the pathogenesis of colorectal cancer is supported by its critical role in the differentiation of stem cells in intestinal crypts and in the maintenance of intestinal homeostasis. For this review, we will focus on the development of adenomatous polyps through the interplay between renewal signaling in the colon epithelium and reactive oxygen species (ROS) production. The current knowledge of molecular pathology allows us to deepen the relationships between oxidative stress and other risk factors as lifestyle, microbiota, and predisposition. We underline that the chronic inflammation and ROS production in the colon epithelium can impair the Wnt/β-catenin and/or base excision repair (BER) pathways and predispose to polyp development. In fact, the coexistence of oxidative DNA damage and errors in DNA polymerase can foster C>T transitions in various types of cancer and adenomas, leading to a hypermutated phenotype of tumor cells. Moreover, the function of Adenomatous Polyposis Coli (APC) protein in regulating DNA repair is very important as therapeutic implication making DNA damaging chemotherapeutic agents more effective in CRC cells that tend to accumulate mutations. Additional studies will determine whether approaches based on Wnt inhibition would provide long-term therapeutic value in CRC, but it is clear that APC disruption plays a central role in driving and maintaining tumorigenesis.

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Gut as a target for cadmium toxicity

Cited by 187 publications

References 66 publications

Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Cadmium‐induced toxicity increases prolyl endopeptidase (PREP) expression in the rat testis

Molecular Aspects of Colorectal Adenomas: The Interplay among Microenvironment, Oxidative Stress, and Predisposition

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