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      Effects of Cadmium, Lead, and Mercury on the Structure and Function of Reproductive Organs

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          Abstract

          Reproductive organs are essential not only for the life of an individual but also for the survival and development of the species. The response of reproductive organs to toxic substances differs from that of other target organs, and they may serve as an ideal “barometer” for the deleterious effects of environmental pollution on animal and human health. The incidence of infertility, cancers, and associated maladies has increased in the last fifty years or more, while various anthropogenic activities have released into the environment numerous toxic substances, including cadmium, lead, and mercury. Data from epidemiological studies suggested that environmental exposure to cadmium, lead, and mercury may have produced reproductive and developmental toxicity. The present review focused on experimental studies using rats, mice, avian, and rabbits to demonstrate unambiguously effects of cadmium, lead, or mercury on the structure and function of reproductive organs. In addition, relevant human studies are discussed. The experimental studies reviewed have indicated that the testis and ovary are particularly sensitive to cadmium, lead, and mercury because these organs are distinguished by an intense cellular activity, where vital processes of spermatogenesis, oogenesis, and folliculogenesis occur. In ovaries, manifestation of toxicity induced by cadmium, lead, or mercury included decreased follicular growth, occurrence of follicular atresia, degeneration of the corpus luteum, and alterations in cycle. In testes, toxic effects following exposure to cadmium, lead, or mercury included alterations of seminiferous tubules, testicular stroma, and decrease of spermatozoa count, motility and viability, and aberrant spermatozoa morphology.

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          The Effects of Cadmium Toxicity

          Cadmium (Cd) is a toxic non-essential transition metal that poses a health risk for both humans and animals. It is naturally occurring in the environment as a pollutant that is derived from agricultural and industrial sources. Exposure to cadmium primarily occurs through the ingestion of contaminated food and water and, to a significant extent, through inhalation and cigarette smoking. Cadmium accumulates in plants and animals with a long half-life of about 25–30 years. Epidemiological data suggest that occupational and environmental cadmium exposure may be related to various types of cancer, including breast, lung, prostate, nasopharynx, pancreas, and kidney cancers. It has been also demonstrated that environmental cadmium may be a risk factor for osteoporosis. The liver and kidneys are extremely sensitive to cadmium’s toxic effects. This may be due to the ability of these tissues to synthesize metallothioneins (MT), which are Cd-inducible proteins that protect the cell by tightly binding the toxic cadmium ions. The oxidative stress induced by this xenobiotic may be one of the mechanisms responsible for several liver and kidney diseases. Mitochondria damage is highly plausible given that these organelles play a crucial role in the formation of ROS (reactive oxygen species) and are known to be among the key intracellular targets for cadmium. When mitochondria become dysfunctional after exposure to Cd, they produce less energy (ATP) and more ROS. Recent studies show that cadmium induces various epigenetic changes in mammalian cells, both in vivo and in vitro, causing pathogenic risks and the development of various types of cancers. The epigenetics present themselves as chemical modifications of DNA and histones that alter the chromatin without changing the sequence of the DNA nucleotide. DNA methyltransferase, histone acetyltransferase, histone deacetylase and histone methyltransferase, and micro RNA are involved in the epigenetic changes. Recently, investigations of the capability of sunflower (Helianthus annuus L.), Indian mustard (Brassica juncea), and river red gum (Eucalyptus camaldulensis) to remove cadmium from polluted soil and water have been carried out. Moreover, nanoparticles of TiO2 and Al2O3 have been used to efficiently remove cadmium from wastewater and soil. Finally, microbial fermentation has been studied as a promising method for removing cadmium from food. This review provides an update on the effects of Cd exposure on human health, focusing on the cellular and molecular alterations involved.
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            Cadmium, Environmental Exposure, and Health Outcomes

            Objectives We provide an update of the issues surrounding health risk assessment of exposure to cadmium in food. Data sources We reviewed epidemiologic studies published between 2004 and 2009 concerning the bioavailability of cadmium in food, assessment of exposure, and body burden estimate, along with exposure-related effects in nonoccupationally exposed populations. Data extraction and synthesis Bioavailability of ingested cadmium has been confirmed in studies of persons with elevated dietary exposure, and the findings have been strengthened by the substantial amounts of cadmium accumulated in kidneys, eyes, and other tissues and organs of environmentally exposed individuals. We hypothesized that such accumulation results from the efficient absorption and systemic transport of cadmium, employing multiple transporters that are used for the body’s acquisition of calcium, iron, zinc, and manganese. Adverse effects of cadmium on kidney and bone have been observed in environmentally exposed populations at frequencies higher than those predicted from models of exposure. Increasing evidence implicates cadmium in the risk of diseases that involve other tissues and organ systems at cadmium concentrations that do not produce effects on bone or renal function. Conclusions Population data raise concerns about the validity of the current safe intake level that uses the kidney as the sole target in assessing the health risk from ingested cadmium. The data also question the validity of incorporating the default 5% absorption rate in the threshold-type risk assessment model, known as the provisional tolerable weekly intake (PTWI), to derive a safe intake level for cadmium.
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              Lead Toxicity: Health Hazards, Influence on Food Chain, and Sustainable Remediation Approaches

              Lead (Pb) toxicity has been a subject of interest for environmental scientists due to its toxic effect on plants, animals, and humans. An increase in several Pb related industrial activities and use of Pb containing products such as agrochemicals, oil and paint, mining, etc. can lead to Pb contamination in the environment and thereby, can enter the food chain. Being one of the most toxic heavy metals, Pb ingestion via the food chain has proven to be a potential health hazard for plants and humans. The current review aims to summarize the research updates on Pb toxicity and its effects on plants, soil, and human health. Relevant literature from the past 20 years encompassing comprehensive details on Pb toxicity has been considered with key issues such as i) Pb bioavailability in soil, ii) Pb biomagnification, and iii) Pb- remediation, which has been addressed in detail through physical, chemical, and biological lenses. In the review, among different Pb-remediation approaches, we have highlighted certain advanced approaches such as microbial assisted phytoremediation which could possibly minimize the Pb load from the resources in a sustainable manner and would be a viable option to ensure a safe food production system.
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                Author and article information

                Journal
                Toxics
                Toxics
                toxics
                Toxics
                MDPI
                2305-6304
                29 October 2020
                December 2020
                : 8
                : 4
                : 94
                Affiliations
                [1 ]Department of Animal Physiology, Slovak University of Agriculture in Nitra, Tr. A. Hlinku 2, SK 94976 Nitra, Slovakia; norbert.lukac@ 123456uniag.sk
                [2 ]Institute of Biology, Pedagogical University of Kraków, ul. Podchorążych 2, 30-084 Kraków, Poland; robert.stawarz@ 123456gmail.com
                [3 ]Department of Animal Husbandry, Slovak University of Agriculture in Nitra, Tr. A. Hlinku 2, SK 94976 Nitra, Slovakia; martinmassanyi@ 123456yahoo.com
                [4 ]Department of Biomedical Sciences-Histology, University of Sassari, Viale San Pietro 43/B, 07100 Sassari, Italy; rmadeddu@ 123456uniss.it
                Author notes
                [* ]Correspondence: peter.massanyi@ 123456uniag.sk ; Tel.: +421-37-641-4284
                Author information
                https://orcid.org/0000-0002-4216-0948
                https://orcid.org/0000-0002-9281-4495
                Article
                toxics-08-00094
                10.3390/toxics8040094
                7711607
                33137881
                476577c5-4fc5-4562-8f50-661d8166e772
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 21 August 2020
                : 23 October 2020
                Categories
                Review

                toxic metals,cadmium,lead,mercury,reproduction,testicular and ovarian structure

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