Study of the influence of the ph of water in the initiation of digestive tract injury in cadmium poisoning in rats

Nai, Gisele Alborghetti; Filho, Mozart Alves Gonçalves; Estrella, Mariani Paulino Soriano; Teixeira, Larissa Di Santi

doi:10.1016/j.toxrep.2015.07.012

Cited by 15 publications

(7 citation statements)

References 30 publications

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“…Studies have shown that the pH of drinking water (5.0, 7.0, and 8.0) does not seem to affect the lesions in the digestive tract caused by Cd poisoning [ 26 ]. Although blood Cd levels are significantly higher in GI cancer patients compared with healthy individuals, a multivariate regression model did not reveal a significant correlation between blood Cd concentrations and the risk of GI cancer [ 65 ].…”

Section: Discussionmentioning

confidence: 99%

“…One study reported that Cd exposure led to intestinal inflammation and tissue damage. It has been recently reported that chronic Cd exposure resulted in the formation of dysplastic lesions in gastric glandular epithelium but that it did not damage the esophageal and intestinal epithelium [ 26 ]. When rats were exposed to 15 ppm CdCl 2 for 30 days, mean blood and mucosa Cd levels significantly increased ( P < 0.01 and P < 0.001, resp.…”

Section: Mechanisms Of Heavy Metal Carcinogenicity In the Stomachmentioning

confidence: 99%

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Advances in Understanding How Heavy Metal Pollution Triggers Gastric Cancer

Wang

Yang

2016

BioMed Research International

124

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With the development of industrialization and urbanization, heavy metals contamination has become a major environmental problem. Numerous investigations have revealed an association between heavy metal exposure and the incidence and mortality of gastric cancer. The mechanisms of heavy metals (lead, cadmium, mercury, chromium, and arsenic) contamination leading to gastric cancer are concluded in this review. There are four main potential mechanisms: (1) Heavy metals disrupt the gastric mucosal barrier by decreasing mucosal thickness, mucus content, and basal acid output, thereby affecting the function of E-cadherin and inducing reactive oxygen species (ROS) damage. (2) Heavy metals directly or indirectly induce ROS generation and cause gastric mucosal and DNA lesions, which subsequently alter gene regulation, signal transduction, and cell growth, ultimately leading to carcinogenesis. Exposure to heavy metals also enhances gastric cancer cell invasion and metastasis. (3) Heavy metals inhibit DNA damage repair or cause inefficient lesion repair. (4) Heavy metals may induce other gene abnormalities. In addition, heavy metals can induce the expression of proinflammatory chemokine interleukin-8 (IL-8) and microRNAs, which promotes tumorigenesis. The present review is an effort to underline the human health problem caused by heavy metal with recent development in order to garner a broader perspective.

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Section: Discussionmentioning

confidence: 99%

Section: Mechanisms Of Heavy Metal Carcinogenicity In the Stomachmentioning

confidence: 99%

Advances in Understanding How Heavy Metal Pollution Triggers Gastric Cancer

Wang

Yang

2016

BioMed Research International

124

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“…Long time exposure to lead increases the risk of Alzheimer's disease in the elderly [45]. Acute cadmium poisoning usually occurs 12-24 hours after exposure, with severe respiratory symptoms and necrosis of the liver and kidney, while chronic cadmium poisoning is mainly characterized by toxicity in the cardiovascular, cerebrovascular, kidney, and digestive tract [46][47][48][49]. Mercury volatilizes easily and chronic exposure to mercury causes nervous system damage and visual impairment, which poses a high level of risk in certain occupations [50][51][52][53].…”

Section: Discussionmentioning

confidence: 99%

Exposure to Heavy Metal Elements May Significantly Increase Serum Prostate-Specific Antigen Levels With Overdosed Dietary Zinc

Chen

Song

et al. 2021

Preprint

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Background: Serum prostate-specific antigen (PSA) is a primary metric for diagnosis and prognosis of prostate cancer (PCa). Exposure to heavy metals, such as lead, cadmium, mercury, and zinc can impact PSA levels in PCa patients. However, it is unclear whether this effect also occurs in men without PCa, which may lead to the overdiagnosis of PCa.Method: Data on a total of 5,089 American men who had never been diagnosed with PCa were obtained from the National Health and Nutrition Examination Survey performed from 2003–2010. The relationship between serum PSA levels (dependent variable) and concentrations of lead (μmol/L), cadmium (nmol/L), and mercury (μmol/L) were investigated with dietary zinc intake being used as a potential modifier or covariate in a weighted linear regression model and a generalized additive model. A series of bootstrapping analyses were performed to evaluate sensitivity and specificity using these models. Results: Regression analyses suggested that, in general, lead, cadmium, or mercury did not show an association with PSA levels, which was consistent with the results of the bootstrapping analyses. However, in a subgroup of participants with a high level of dietary zinc intake (≥14.12 mg/day), a significant positive association between cadmium and serum PSA was identified (1.06, 95% CI, P=0.0268, P for interaction=0.0249).Conclusions: With high-level zinc intake, serum PSA levels may rise in PCa-free men as the exposure to cadmium increases, leading to a potential risk of an overdiagnosis of PCa and unnecessary treatment. Therefore, environmental variables should be factored in the current diagnostic model for PCa that is solely based on PSA measurements. Different criteria for PSA screening are necessary based on geographical variables. Further investigations are needed to uncover the biological and biochemical relationship between zinc, cadmium, and serum PSA levels to more precisely diagnose PCa.

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“…Three serial cuts from each organ were analyzed. The general parameters evaluated in the esophagus, stomach, and small and large intestines with their respective scores were interstitial inflammatory infiltrate (0=absent, 1=mild, 2=moderate, 3=intense) and type of inflammatory cell present (polymorphonuclear and/or mononuclear); tissue congestion (0=absent, 1=mild, 2=moderate, 3=severe); tissue necrosis (0=absent; 1=present and focal, 2=present and diffuse); vascular necrosis (0=absent, 1=present); non-neoplastic changes in the mucosa (atrophy, hyperplasia; 0=absent, 1=present); dysplastic lesions (0=absent, 1=mild dysplasia, 2=moderate dysplasia, 3=severe dysplasia), and presence of benign and malignant neoplastic lesions (0=absent, 1=benign, 2=malignant) ( 9 ).…”

Section: Methodsmentioning

confidence: 99%

Digestive tract toxicity associated with exposure to 2,4-dichlorophenoxyacetic acid in rats

Mariotti

Naufal

Amorim

et al. 2022

Braz J Med Biol Res

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2,4-Dichlorophenoxyacetic acid (2,4-D) is a herbicide of the chlorophenoxy class and the second most widely used herbicide applied to several different crops worldwide. Environmental factors, especially those related to diet, strongly affect the risk of developing cancer of the gastrointestinal tract. There is currently no evidence to determine whether there is an association between 2,4-D exposure and gastrointestinal disorders. We evaluated the histological effect of chronic oral and inhalation exposure to 2,4-D on the digestive tract of rats. Eighty male adult albino Wistar rats were divided into 8 groups (n=10): two control groups, one for inhalation and one for oral exposure, and 6 groups exposed orally or by inhalation at three different concentrations of 2,4-D [3.71×10 -3 grams of active ingredient per hectare (gai/ha), 6.19×10 -3 gai/ha, and 9.28×10 -3 gai/ha]. The animals were exposed for 6 months. The esophagus, stomach, and intestine were collected for histopathological analysis. Animals exposed to 2,4-D had hyperkeratosis of the esophagus, regardless of the exposure route. All animals exposed to a higher concentration of 2,4-D orally presented mild dysplasia of the large intestine. In the small intestine, most animals exposed to moderate and high concentrations of 2,4-D had mild dysplasia. No gastric changes were observed in any of the groups studied. Chronic exposure to 2,4-D, especially at moderate and high concentrations, regardless of the exposure route, caused reactive damage to the esophagus (hyperkeratosis) and dysplastic changes to the intestine.

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Study of the influence of the ph of water in the initiation of digestive tract injury in cadmium poisoning in rats

Cited by 15 publications

References 30 publications

Advances in Understanding How Heavy Metal Pollution Triggers Gastric Cancer

Advances in Understanding How Heavy Metal Pollution Triggers Gastric Cancer

Exposure to Heavy Metal Elements May Significantly Increase Serum Prostate-Specific Antigen Levels With Overdosed Dietary Zinc

Digestive tract toxicity associated with exposure to 2,4-dichlorophenoxyacetic acid in rats

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