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Review
. 2024 Mar 20;12(3):226.
doi: 10.3390/toxics12030226.

Single-Nucleotide Polymorphisms Associated with Mercury Levels and Neurological Symptoms: An Overview

Jamila Alessandra Perini  1   2 , Jessica Vilarinho Cardoso  1 , Alana de Oliveira Knesse  1 , Felipe Oliveira Pessoa-Silva  1 , Ana Claudia Santiago de Vasconcellos  2 , Daniel Escorsim Machado  1 , Paulo Cesar Basta  3   4
Affiliations
Review

Single-Nucleotide Polymorphisms Associated with Mercury Levels and Neurological Symptoms: An Overview

Jamila Alessandra Perini et al. Toxics. .

Abstract

Mercury (Hg) pollution is a global public health concern because of its adverse effects on the environment and health. Single-nucleotide polymorphisms (SNPs) have been associated with Hg levels and outcomes. The aim of this review was to describe the research and discuss the evidence on the genetic susceptibility of Hg-exposed individuals to the development of neurocognitive disorders. A systematic review was performed to identify the genes/SNPs associated with Hg toxicokinetics and that, therefore, affect neurological function in exposed populations. Observational and experimental studies were identified by screening three databases. Thirteen articles were included (quality score 82-100%) and 8124 individuals were evaluated. Hg exposure was mainly fish consumption (77%) and, in 31% of the studies, the Hg levels exceeded the reference limits. Genetic susceptibility to higher Hg levels and neurotoxicity risk in Hg poisoning were associated with eight (ALAD rs1800435, CYP3A4 rs2740574, CYP3A5 rs776746, CYP3A7 rs2257401, GSTP1 rs1695, MT1A rs8052394, MT1M rs2270836, and MT4 rs11643815) and three (MT1A rs8052394, MT1M rs2270837, and MT2A rs10636) SNPs, respectively, and rs8052394 was associated with both outcomes. The MT1A rs8052394 SNP may be used as a susceptibility biomarker to identify individuals at greater risk for higher Hg levels and the development of neurocognitive disorders in metal-exposed populations.

Keywords: environmental health; genetic polymorphism; mercury exposure; mercury poisoning; neurotoxicity; toxicokinetic.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The mechanistic model to explain the basic concepts of genetic inheritance and single-nucleotide polymorphism. (A) Organization of human genome information in the cell. (B) Example of the rs1800435 SNP in the ALAD gene. (C) Example of three different genotypes of the ALAD rs1800435 SNP (CC, CG, and GG) and their corresponding phenotypes (normal and poor metabolizers). (D) Example of neurological outcomes caused by carrying the ALAD rs1800435 SNP. Legend: SNP = single-nucleotide polymorphism.
Figure 2
Figure 2
Flowchart of the literature search, screening, eligibility, exclusion, and inclusion of articles evaluated in this review.
Figure 3
Figure 3
Mechanistic model to explaining the basic concepts of genes/SNPs associated with genetic susceptibility to any neurological changes in individuals exposed to mercury poisoning. Legend: MDI = mental development index. Mercury exposure routes: fish consumption, use of dental amalgams, and occupational exposure. CYP3A SNPs were inversely associated with increased Hg levels and increased MDI scores. The MT1A SNP was associated with higher Hg levels and cognitive impairment in Hg poisoning. The MT1M and MT2A SNPs were associated with negative changes for the neurobehavioral functions associated with Hg exposure among boys.
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References

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