For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
15
views
53
references
 Top references
cited by
16
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      339
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Role of Lead and Cadmium in Psychiatry

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Psychiatric disorders are associated with long-term disability and huge social and economic costs. The possible influence of heavy metals exposure on public health remains a matter of concern. A recurring research question that persisted among researchers in neuropsychiatry has been “are psychiatric patients more likely to have a high body burden of lead or other heavy metals?” This is an update account on the role of lead and cadmium in psychiatry. This review, which has employed search words like “lead and cadmium in psychiatry”, “lead and cadmium in schizophrenia”, “lead and cadmium in psychosis” in citation indices such as PubMed, Google Scholar, Scirus, and Scopus. A total of 415 articles were found; 60 fulfiled the inclusion criteria. Evidence-based information suggests that lead and cadmium may be involved in psychiatry. Should environmental lead and cadmium be implicated in the etiogenesis of psychiatry given the characteristic high environmental pollution in Sub Sahara Africa, it is worthwhile for toxicologists and scientists in Sub-Sahara Africa to investigate if lead and cadmium can become additional biomarkers in the diagnosis of psychiatric disorders.

          Related collections

          Most cited references53

          • Record: found
          • Abstract: found
          • Article: not found

          Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative-antioxidative systems.

          Asli Sarandol, Emre Sarandol, Salih Saygin Eker … (2007)
          The aim of the present study was to investigate the oxidative-antioxidative systems and effects of different antidepressants on these systems in patients with major depressive disorder (MDD). Ninety-six patients with a Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV) diagnosis of MDD and 54 healthy controls were included in the study. Plasma malondialdehyde (MDA) levels and susceptibility of red blood cells (RBCs) to oxidation were determined to investigate the oxidative status, plasma vitamin E, vitamin C, serum total carotenoid levels, total antioxidant capacity (TAOC), RBC superoxide dismutase (SOD) and whole blood glutathione peroxidase (GPx) activities were measured to investigate the antioxidative defence before and after 6 weeks of antidepressant treatment. Plasma MDA levels and susceptibility of RBCs to oxidation were significantly higher in the MDD group compared with the control group. RBC SOD activity was significantly increased in patients with MDD, and furthermore there was a significant positive correlation between the severity of the disease and SOD activity. MDD is accompanied with oxidative stress; however, oxidative-antioxidative systems do not seem to be affected by 6 weeks of antidepressant treatment. Copyright (c) 2007 John Wiley & Sons, Ltd.
          Article 0 comments Cited 140 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Antioxidant nutrients and lead toxicity.

            P. Hsu, Yue Leon GUO (2002)
            Lead-induced oxidative stress contributes to the pathogenesis of lead poisoning for disrupting the delicate prooxidant/antioxidant balance that exists within mammalian cells. Production of reactive oxygen species (ROS) is increased after lead treatment in in vitro studies. In vivo studies suggest that lead exposure causes generation of ROS and alteration of antioxidant defense systems in animals and occupationally exposed workers. The mechanisms for lead-induced oxidative stress include the effect of lead on membrane, DNA, and antioxidant defense systems of cells. From low to high doses of lead exposure, there are different responses of lead-induced oxidative stress in various target sites including lung, blood vessels, testes, sperm, liver, and brain in epidemiological as well as animal studies. Therefore, reducing the possibility of lead interacting with critical biomolecules and inducing oxidative damage, or bolstering the cell's antioxidant defenses might be associated with the beneficial role of antioxidant nutrients through exogenous supplementation of antioxidant molecules. Although many researchers have investigated the benefit of antioxidants in preventing lead toxicity, the mechanisms of antioxidant nutrients being effective via rebalancing the impaired prooxidant/antioxidant ratio are not completely clear. Antioxidant nutrients including, vitamin E, vitamin C, vitamin B(6), beta-carotene, zinc, and selenium, are addressed in this review to discuss their beneficial role in lead-induced oxidative stress.
            Article 0 comments Cited 95 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mechanisms of lead-induced hypertension and cardiovascular disease.

              N. Vaziri (2008)
              Lead is a ubiquitous environmental toxin that is capable of causing numerous acute and chronic illnesses. Population studies have demonstrated a link between lead exposure and subsequent development of hypertension (HTN) and cardiovascular disease. In vivo and in vitro studies have shown that chronic lead exposure causes HTN and cardiovascular disease by promoting oxidative stress, limiting nitric oxide availability, impairing nitric oxide signaling, augmenting adrenergic activity, increasing endothelin production, altering the renin-angiotensin system, raising vasoconstrictor prostaglandins, lowering vasodilator prostaglandins, promoting inflammation, disturbing vascular smooth muscle Ca(2+) signaling, diminishing endothelium-dependent vasorelaxation, and modifying the vascular response to vasoactive agonists. Moreover, lead has been shown to cause endothelial injury, impede endothelial repair, inhibit angiogenesis, reduce endothelial cell growth, suppress proteoglycan production, stimulate vascular smooth muscle cell proliferation and phenotypic transformation, reduce tissue plasminogen activator, and raise plasminogen activator inhibitor-1 production. Via these and other actions, lead exposure causes HTN and promotes arteriosclerosis, atherosclerosis, thrombosis, and cardiovascular disease. In conclusion, studies performed in experimental animals, isolated tissues, and cultured cells have provided compelling evidence that chronic exposure to low levels of lead can cause HTN, endothelial injury/dysfunction, arteriosclerosis, and cardiovascular disease. More importantly, these studies have elucidated the cellular and molecular mechanisms of lead's action on cardiovascular/renal systems, a task that is impossible to accomplish using clinical and epidemiological investigations alone.
              Article 0 comments Cited 91 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): N Am J Med Sci
                Journal ID (iso-abbrev): N Am J Med Sci
                Journal ID (publisher-id): NAJMS
                Title: North American Journal of Medical Sciences
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2250-1541
                ISSN (Electronic): 1947-2714
                Publication date (Print): August 2014
                Volume: 6
                Issue: 8
                Pages: 370-376
                Affiliations
                [1] Department of Experimental Pharmacology and Clinical Pharmacy, Toxicology Unit, Clinical Pharmacy, Faculty of Pharmacy, University of Port-Hacourt, Rivers State, Nigeria
                Author notes
                Address for correspondence: Prof. Orish Ebere Orisakwe, Toxicology Unit, Clinical Pharmacy, Faculty of Pharmacy, University of Port-Hacourt, Rivers, Nigeria. E-mail: orishebere@ 123456gmail.com
                Article
                Publisher ID: NAJMS-6-370
                DOI: 10.4103/1947-2714.139283
                PMC ID: 4158644
                PubMed ID: 25210669
                SO-VID: c6cb7d6d-ee7f-468c-9f11-95ba6b2ac623
                Copyright © Copyright: © North American Journal of Medical Sciences
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Medicine
                Keywords: cadmium,environmental health,lead,psychiatry
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: cadmium, environmental health, lead, psychiatry

                Comments

                Comment on this article

                scite_

                Similar content339

                See all similar

                Cited by16

                See all cited by

                Most referenced authors475

                See all reference authors