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      Sperm motility and morphology changes in rats exposed to cadmium and diazinon

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          Abstract

          Background

          Humans are ubiquitously exposed to multiple environmental contaminants. Consequences of combined action on the reproductive system remain unknown. This study aimed to assess single and joint effects of cadmium and diazinon exposure on sperm quality parameters.

          Methods

          Male adult Wistar rats were randomized into 4 groups of ten animals each. Group A was used as a control, animals from group B were exposed to cadmium (30 mg/L), rats from group C were administered with diazinon (40 mg/L), and rats from group D were exposed simultaneously to cadmium (30 mg/L) and diazinon (40 mg/L) via drinking water for 90 days. Sperm morphology and motility were evaluated using a bright field microscope and a computer-assisted semen analysis.

          Results

          The percentage of motile spermatozoa and morphologically normal sperm was markedly reduced in rats from the group B. Rats from the C group showed an increase in velocity parameters, amplitude of lateral head displacement, decrease in beat-cross frequency, and an increase in abnormal sperm morphology. Simultaneous coexposure to cadmium and diazinon increased distance and velocity parameters, and amplitude of lateral head displacement. Reductions were observed in straightness, linearity, wobble, and beat-cross frequency. The decreased normal sperm morphology rates were related to defects of the sperm tail.

          Conclusions

          Exposure to cadmium and diazinon at relatively low doses impairs sperm quality and can reduce male fertility. Cadmium and diazinon caused significant changes on sperm morphology with varying effects on motility patterns. These parameters were significantly higher in the group D as compared to the group C. The findings have important implications for reproductive risk assessment of combined exposures to multiple chemicals.

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          Most cited references43

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          Current status of cadmium as an environmental health problem.

          Cadmium is a toxic metal occurring in the environment naturally and as a pollutant emanating from industrial and agricultural sources. Food is the main source of cadmium intake in the non-smoking population. The bioavailability, retention and toxicity are affected by several factors including nutritional status such as low iron status. Cadmium is efficiently retained in the kidney (half-time 10-30 years) and the concentration is proportional to that in urine (U-Cd). Cadmium is nephrotoxic, initially causing kidney tubular damage. Cadmium can also cause bone damage, either via a direct effect on bone tissue or indirectly as a result of renal dysfunction. After prolonged and/or high exposure the tubular injury may progress to glomerular damage with decreased glomerular filtration rate, and eventually to renal failure. Furthermore, recent data also suggest increased cancer risks and increased mortality in environmentally exposed populations. Dose-response assessment using a variety of early markers of kidney damage has identified U-Cd points of departure for early kidney effects between 0.5 and 3 microg Cd/g creatinine, similar to the points of departure for effects on bone. It can be anticipated that a considerable proportion of the non-smoking adult population has urinary cadmium concentrations of 0.5 microg/g creatinine or higher in non-exposed areas. For smokers this proportion is considerably higher. This implies no margin of safety between the point of departure and the exposure levels in the general population. Therefore, measures should be put in place to reduce exposure to a minimum, and the tolerably daily intake should be set in accordance with recent findings.
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            Molecular and cellular mechanisms of cadmium carcinogenesis.

            Cadmium is a heavy metal, which is widely used in industry, affecting human health through occupational and environmental exposure. In mammals, it exerts multiple toxic effects and has been classified as a human carcinogen by the International Agency for Research on Cancer. Cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities. Cd2+ does not catalyze Fenton-type reactions because it does not accept or donate electrons under physiological conditions, and it is only weakly genotoxic. Hence, indirect mechanisms are implicated in the carcinogenicity of cadmium. In this review multiple mechanisms are discussed, such as modulation of gene expression and signal transduction, interference with enzymes of the cellular antioxidant system and generation of reactive oxygen species (ROS), inhibition of DNA repair and DNA methylation, role in apoptosis and disruption of E-cadherin-mediated cell-cell adhesion. Cadmium affects both gene transcription and translation. The major mechanisms of gene induction by cadmium known so far are modulation of cellular signal transduction pathways by enhancement of protein phosphorylation and activation of transcription and translation factors. Cadmium interferes with antioxidant defense mechanisms and stimulates the production of reactive oxygen species, which may act as signaling molecules in the induction of gene expression and apoptosis. The inhibition of DNA repair processes by cadmium represents a mechanism by which cadmium enhances the genotoxicity of other agents and may contribute to the tumor initiation by this metal. The disruption of E-cadherin-mediated cell-cell adhesion by cadmium probably further stimulates the development of tumors. It becomes clear that there exist multiple mechanisms which contribute to the carcinogenicity of cadmium, although the relative weights of these contributions are difficult to estimate.
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              Current issues in organophosphate toxicology.

              Organophosphates (OPs) are one of the main classes of insecticides, in use since the mid 1940s. OPs can exert significant adverse effects in non-target species including humans. Because of the phosphorylation of acetylcholinesterase, they exert primarily a cholinergic toxicity, however, some can also cause a delayed polyneuropathy. Currently debated and investigated issues in the toxicology of OPs are presented in this review. These include: 1) possible long-term effects of chronic low-level exposures; 2) genetic susceptibility to OP toxicity; 3) developmental toxicity and neurotoxicity; 4) common mechanism of action; 5) mechanisms of delayed neurotoxicity; and 6) possible additional OP targets. Continuing and recent debates, and molecular advances in these areas, and their contributions to our understanding of the toxicology of OPs are discussed.
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                Author and article information

                Contributors
                madamkovicova@ukf.sk
                robert.toman@uniag.sk
                mmartiniakova@ukf.sk
                romelka@ukf.sk
                ramona.babosova@ukf.sk
                vkrajcovicova@ukf.sk
                birgit.grosskopf@biologie.uni-goettingen.de
                peter.massanyi@uniag.sk
                Journal
                Reprod Biol Endocrinol
                Reprod. Biol. Endocrinol
                Reproductive Biology and Endocrinology : RB&E
                BioMed Central (London )
                1477-7827
                8 August 2016
                8 August 2016
                2016
                : 14
                : 42
                Affiliations
                [1 ]Department of Botany and Genetics, Constantine the Philosopher University, 949 74 Nitra, Slovakia
                [2 ]Department of Veterinary Disciplines, Slovak University of Agriculture, 949 76 Nitra, Slovakia
                [3 ]Department of Zoology and Anthropology, Constantine the Philosopher University, 949 74 Nitra, Slovakia
                [4 ]Institute of Zoology and Anthropology, Georg-August University, 37 073 Göttingen, Germany
                [5 ]Department of Animal Physiology, Slovak University of Agriculture, 949 76 Nitra, Slovakia
                Article
                177
                10.1186/s12958-016-0177-6
                4977869
                27503218
                96914fe3-9f8a-42cc-94dc-fe0e6f70e2ba
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 17 June 2016
                : 28 July 2016
                Funding
                Funded by: Ministry of Education, Slovakia
                Award ID: AgroBioTech ITMS 26220220180
                Award ID: KEGA 031UKF-4/2016
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Human biology
                sperm,motility,morphology,rat,cadmium,diazinon
                Human biology
                sperm, motility, morphology, rat, cadmium, diazinon

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