Cadmium, Organ Toxicity and Therapeutic Approaches: A Review on Brain, Kidney and Testis Damage

Rinaldi, Mariagrazia; Micali, Antonio; Marini, Herbert; Adamo, Elena Bianca; Puzzolo, Domenico; Pisani, Antonina; Trichilo, Vincenzo; Altavilla, Domenica; Squadrito, Francesco; Minutoli, Letteria

doi:10.2174/0929867324666170801101448

Cited by 121 publications

(52 citation statements)

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“…Neurotoxic effects may play a key role in the systemic toxic consequences of Cd exposure [ 45 ]. Therefore, the mechanism of Cd neurotoxicity should be better clarified, and measures should be taken to reduce Cd exposure in the general population to minimize the risk of adverse human health effects [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Polydeoxyribonucleotide in a Murine Model of Cadmium Toxicity

Marini

Puzzolo

Micali

et al. 2018

Oxidative Medicine and Cellular Longevity

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Cadmium (Cd) is a harmful heavy metal, which causes severe brain damage and neurotoxic effects. Polydeoxyribonucleotide (PDRN) stimulates adenosine A2A receptor, thus contrasting several deleterious mechanisms in course of tissue damages. We aimed to investigate the possible neuroprotective effect of PDRN in a murine model of Cd-induced brain toxicity. Male C57 BL/6J mice were treated as follows: vehicle (0.9% NaCl, 1 ml/kg/day), PDRN (8 mg/kg/day), CdCl2 (2 mg/kg/day), and CdCl2 + PDRN. Animals were tested with the Morris water maze test to assess spatial memory and learning. After 14 days of treatment, brains were processed to evaluate the presence of edema in the cerebral tissue, the expression of mammalian target of rapamycin kinase (mTOR) and brain-derived neurotrophic factor (BDNF), and the morphological behavior of the hippocampal structures. After CdCl2 administration, the escape latency was high, protein expression of BDNF was significantly decreased if compared to controls, mTOR levels were higher than normal controls, and brain edema and neuronal damages were evident. The coadministration of CdCl2 and PDRN significantly diminished the escape latency, increased BDNF levels, and decreased protein expression of mTOR. Furthermore, brain edema was reduced and the structural organization and the number of neurons, particularly in the CA1 and CA3 hippocampal areas, were improved. In conclusion, a functional, biochemical, and morphological protective effect of PDRN against Cd induced toxicity was demonstrated in mouse brain.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Polydeoxyribonucleotide in a Murine Model of Cadmium Toxicity

Marini

Puzzolo

Micali

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…In fact, increasing research indicates that environmental exposure to Cd is related to poor semen quality and male infertility 8 . Previously, the studies of Cd-induced damage to male testes focus on high-dose acute Cd exposure, which impairs the blood-testis barrier 9 and leydig cells (LCs) regeneration 10 , causing a large amount of germ cell death 11 . Nonetheless, no study to date has investigated the cross-talk between apoptosis and autophagy in testicular injury/self-repair induced by low-dose continuous Cd exposure.…”

Section: Introductionmentioning

confidence: 99%

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Wang

et al. 2020

Cell Death Dis

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Autophagy and apoptosis are two major modes of cell death. A balanced interplay between both is vital for phagocytic clearance of apoptotic testicular cells. Here, generating a SD rats model-treated with cadmium (Cd) to mimic environmental exposure on human, we show that autophagy and apoptosis present synchronous change trends in Cd-induced testicular injury/self-recovery. Further, the cross-talk of autophagy and apoptosis is investigated in four testicular cell lines (GC-1/GC-2/TM3/TM4 cells) respectively. Results reveal that Cd-exposure for five consecutive weeks induces reproductive toxicity in male rats. After one cycle of spermatogenesis within 8 weeks without Cd, toxic effects are ameliorated significantly. In vitro, we find that PI3K inhibitor 3-MA regulates apoptosis by inhibiting autophagy with mTOR-independent pathway in Cd-treated testicular cells. Conclusively, cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by Cd via PI3K with mTOR-independent pathway.

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“…These metals enter the body by oral or inhaled exposure, then they are absorbed, enter into the systemic circulation, and distributed into the organs where they may accumulate. Finally, most of them are eliminated by the kidney, reason why this organ is one of the most affected structures by metals [38]. Also, there are reports that in CKD when there is a problem to eliminate pollutant metals, these can concentrate into kidney cells and the damage worsened when it occurs in humans, both in children and adults [39].…”

Section: Urinary Systemmentioning

confidence: 99%

Oxidative Stress and Vanadium

Rojas-Lemus¹,

Bizarro-Nevares²,

López-Valdéz³

et al. 2021

Genotoxicity and Mutagenicity - Mechanisms and Test Methods

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Air pollution is a worldwide health problem, and metals are one of the various air pollutants to which living creatures are exposed. The pollution by metals such as: lead, cadmium, manganese, and vanadium have a common mechanism of action: the production of oxidative stress in the cell. Oxidative stress favors the production of free radicals, which damage biomolecules such as: DNA, proteins, lipids, and carbohydrates; these free radicals produce changes that are observed in different organs and systems. Vanadium is a transition element delivered into the atmosphere by the combustion of fossil fuels as oxides and adhered to the PM enters into the respiratory system, then crosses the alveolar wall and enters into the systemic circulation. In this chapter, we will review the oxidative stress induced by vanadium-as a common mechanism of metal pollutants-; in addition, we will review the protective effect of the antioxidants (carnosine and ascorbate).

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Cadmium, Organ Toxicity and Therapeutic Approaches: A Review on Brain, Kidney and Testis Damage

Abstract: Nowadays, a therapy able to counteract Cd toxicity is still lacking and the development of new therapeutic agents is requested.

Cited by 121 publications

References 0 publications

Neuroprotective Effects of Polydeoxyribonucleotide in a Murine Model of Cadmium Toxicity

Neuroprotective Effects of Polydeoxyribonucleotide in a Murine Model of Cadmium Toxicity

Cross-talk between autophagy and apoptosis regulates testicular injury/recovery induced by cadmium via PI3K with mTOR-independent pathway

Oxidative Stress and Vanadium

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