Toxic mechanisms of cadmium and exposure as a risk factor for oral and gastrointestinal carcinomas

Tavakoli Pirzaman, Ali; Ebrahimi, Pouyan; Niknezhad, Shokat; vahidi, Turan; Hosseinzadeh, Dariush; Akrami, Sousan; Ashrafi, Arash M; Moeen Velayatimehr, Mohammad; Hosseinzadeh, Rezvan; Kazemi, Sohrab

doi:10.1177/09603271231210262

Cited by 14 publications

(5 citation statements)

References 128 publications

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“…Although, reactive oxygen species (ROS) have a fundamental role in main cellular activities, including signal transduction and bactericidal effect of phagocytes, apoptosis and cellular injury can result from their accumulation. [93][94][95] Besides, a significant part of the chemotherapy-related oxidative damage has been reported to be played by an increase in ROS. [96][97][98] 5FU, as a widely used chemotherapeutic agent, can also produce mitochondrial ROS through the p53-dependent route, and accordingly, it can cause neoplastic cell death.…”

Section: Fu Disrupts Cellular Function By Oxidative Stressmentioning

confidence: 99%

5-Fluorouracil-induced toxicity in both male and female reproductive systems: A narrative review

Pirzaman,

Ebrahimi,

Doostmohamadian

et al. 2023

Hum Exp Toxicol

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The chemotherapeutic drug 5-fluorouracil (5FU) is frequently used to treat a wide range of solid malignant tumors, such as colorectal, pancreatic, gastric, breast, and head and neck cancers. Its antitumoral effects are achieved by interfering with the synthesis of RNA and DNA and by inhibiting thymidylate synthase in both malignant and non-malignant cells. Therefore, it can be responsible for severe toxicities in crucial body organs, including heart, liver, kidney, and reproductive system. Given the fact that 5FU-induced reproductive toxicity may limit the clinical application of this drug, in this study, we aimed to discuss the main locations and mechanisms of the 5FU-induced reproductive toxicity. Initially, we discussed the impact of 5FU on the male reproductive system, which leads to damage of the seminiferous epithelial cells and the development of vacuoles in Sertoli cells. Although no noticeable changes occur at the histopathological level, there is a decrease in the weight of the prostate. Additionally, 5FU causes significant abnormalities in spermatogenesis, including germ cell shedding, spermatid halo formation, polynucleated giant cells, and decreased sperm count. Finally, in females, 5FU-induced reproductive toxicity is characterized by the presence of atretic secondary and antral follicles with reduced numbers of growing follicles, ovarian weight, and maturity impairment.

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Section: Fu Disrupts Cellular Function By Oxidative Stressmentioning

confidence: 99%

5-Fluorouracil-induced toxicity in both male and female reproductive systems: A narrative review

Pirzaman,

Ebrahimi,

Doostmohamadian

et al. 2023

Hum Exp Toxicol

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“…Other types of cancer found to be associated with Cd exposure were endometrial cancer [117], acute myeloid leukemia [118], urinary bladder cancer [119], oral and gastrointestinal carcinomas [120,121], and nasopharyngeal and pharyngeal cancers [122].…”

Section: Cadmium and Other Types Of Cancermentioning

confidence: 99%

Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium

Cirovic,

Satarug

2024

IJMS

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Cadmium (Cd) is an environmental toxicant of worldwide public health significance. Diet is the main non-workplace Cd exposure source other than passive and active smoking. The intestinal absorption of Cd involves transporters for essential metals, notably iron and zinc. These transporters determine the Cd body burden because only a minuscule amount of Cd can be excreted each day. The International Agency for Research on Cancer listed Cd as a human lung carcinogen, but the current evidence suggests that the effects of Cd on cancer risk extend beyond the lung. A two-year bioassay demonstrated that Cd caused neoplasms in multiple tissues of mice. Also, several non-tumorigenic human cells transformed to malignant cells when they were exposed to a sublethal dose of Cd for a prolonged time. Cd does not directly damage DNA, but it influences gene expression through interactions with essential metals and various proteins. The present review highlights the epidemiological studies that connect an enhanced risk of various neoplastic diseases to chronic exposure to environmental Cd. Special emphasis is given to the impact of body iron stores on the absorption of Cd, and its implications for breast cancer prevention in highly susceptible groups of women. Resistance to cell death and other cancer phenotypes acquired during Cd-induced cancer cell transformation, under in vitro conditions, are briefly discussed. The potential role for the ZnT1 efflux transporter in the cellular acquisition of tolerance to Cd cytotoxicity is highlighted.

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“…Cd influences the formation of oral cancer because it changes the apoptotic mechanism in the mucosa [ 7 – 10 ]. In addition, the Cd level was higher in various biological samples, such as hair, blood, and dental calculus, taken from patients with oral cancer than in those from healthy individuals [ 3 , 8 , 11 , 12 ]. Apart from oral cancers, tobacco products (smoke or smokeless) have an important role in the etiology of premalignant white lesions such as oral leukoplakia, which may show hyperkeratosis and epithelial dysplasia [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of tobacco use on cadmium accumulation in the oral keratinized mucosa

Satir,

Kaya,

Ozsoy

2024

BMC Oral Health

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Background This cross-sectional study aimed to evaluate the effect of tobacco use on the accumulation of cadmium (Cd), a carcinogenic element, in the oral keratinized mucosa (OKM). Methods OKM samples were obtained by standard punch biopsy from nonsmokers (n = 19) and smokers (n = 21). Cd analysis was performed using inductively coupled plasma optical emission spectroscopy (ICP-OES). The calibration curve R2 values for three wavelengths (214,439, 226,502, and 228,802 nm) were at the level of 0.9999. The frequency of consumption of foods that are Cd sources, such as seafood, rice, and vegetables, was assessed in all patients. The age, sex, and nutritional habits of all patients and the frequency of tobacco consumption by smokers were recorded. The independent t-test, Mann–Whitney U test, Fisher’s exact test, and Spearman correlation test were used for the statistical analyses, and p < 0.05 was considered significant. Results Although the Cd levels in nonsmokers were higher than those in smokers, no statistically significant difference was found (p > 0.05). In smokers, a positive correlation was found between age and Cd level (r = 0.574, p = 0.006). No significant relationship was found between the groups in terms of nutrition or between the frequency of tobacco consumption and Cd accumulation. Conclusion The OKM may not have the characteristic cumulative accumulation in terms of toxic elements. Changes in the turnover rate, keratinization, and apoptotic mechanisms in the OKM with the thermal/chemical effects of tobacco may be responsible for the difference in Cd accumulation. Trial registration number TCTR20230206001/06 Feb 2023 (TCTR: Thai Clinical Trials Registry).

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Toxic mechanisms of cadmium and exposure as a risk factor for oral and gastrointestinal carcinomas

Cited by 14 publications

References 128 publications

5-Fluorouracil-induced toxicity in both male and female reproductive systems: A narrative review

5-Fluorouracil-induced toxicity in both male and female reproductive systems: A narrative review

Toxicity Tolerance in the Carcinogenesis of Environmental Cadmium

Effect of tobacco use on cadmium accumulation in the oral keratinized mucosa

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