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Toxicology Abstracts

 
 
Every day, in all branches of toxicology, research uncovers new risks associated with the chemicals, pharmaceuticals, and by- products of our age. Toxicology Abstracts is the only comprehensive print resource for professionals in this field who must be aware of every new finding. Specifically focused to meet the needs of toxicologists, Toxicology Abstracts covers issues from social poisons and substance abuse to natural toxins, from legislation and recommended standards to environmental issues. Surveying the literature for toxicology studies of industrial and agricultural chemicals, household products, pharmaceuticals, and myriad other substances, each issue publishes information concerning the in vivo effects of toxic substances. Topics of current concern such as the effects of alcohol and smoking, drug abuse, hydrocarbon studies, nitrosamines, radiation and radioactive materials, and much more are extensively examined. Toxicity testing methodology and analytical procedures for toxic substances are also covered. Through many years of delivering crucial information on the tough, far-reaching issues of toxicology, Toxicology Abstracts has become the single most widely-used journal in this field.

Subject Coverage
    Major areas of coverage include:
    • Pharmaceuticals
    • Food, Additives, and Contaminants
    • Agro-chemicals
    • Cosmetics, Toiletries, and Household Products
    • Industrial Chemicals
    • Metals
    • Toxins and Other Natural Substances
    • Social Poisons and Drug Abuse
    • Polycyclic Hydrocarbons
    • Nitrosamines and Related Compounds
    • Radiation and Radioactive Materials
    • Methodology
    • Legislation and Recommended Standards
Dates of Coverage
    1981 - current
Update Frequency
    Monthly, with approximately 1,030 new records added
Size
    Over 0 records as of May 2013
Print Equivalent
    Toxicology Abstracts
Supplier
    Proquest
    789 E. Eisenhower Parkway
    P.O. Box 1346
    Ann Arbor, MI 48106-1346
    Tel: +1-734-761-4700
Sample Record

    TI:

    Title
    Immune Modulation by Cadmium and Lead in the Acute Reporter Antigen-Popliteal Lymph Node Assay

    AU:

    Author
    Carey, John B; Allshire, Ashley; van Pelt, Frank N

    AF:

    Author Affiliation
    Department of Pharmacology and Therapeutics, University College Cork, Cork, Ireland

    SO:

    Source
    Toxicological Sciences [Toxicol. Sci.]. Vol. 91, no. 1, pp. 113-122. May 2006.

    IS:

    ISSN
    1096-6080

    DE:

    Descriptors
    Metals; Hypersensitivity; Lymphocytes T; Lymph nodes; Immunoglobulin G; Lead; Adjuvants; Cadmium; Autoimmunity; Immunotoxicity; Toxins; Mercury; Lymphocytes B; Immunomodulation; Heavy metals

    AB:

    Abstract
    Immune modulation by heavy metals may cause serious adverse health effects in humans, although the mechanisms involved are not well understood. Both cadmium and lead are important environmental and occupational toxins. Therefore, in the current study, the costimulatory/adjuvant effects and the T-cell-activating potential of these metals (i.e., CdCl sub(2) and PbCl sub(2)), are examined. These immune-modulating properties are critical in the development of conditions such as allergy, hypersensitivity, and autoimmunity. Using the direct popliteal lymph node assay (PLNA) and reporter antigen-popliteal lymph node assay (RA-PLNA) both metals were examined individually for immunotoxicity. Mercury (i.e., HgCl sub(2)) was included for comparative purposes as its effects in the RA-PLNA are well documented. Seven days following a single footpad injection containing metal and/or RA (trinitrophenyl-ovalbumin [TNP-OVA] or TNP-Ficoll), BALB/c mice were sacrificed and the popliteal lymph nodes (PLNs) removed. PLN cellularity, TNP-specific antibody-secreting cells (ASCs), and lymphocyte subsets were assessed. All three metals strongly stimulated T- and B-cell proliferation and ASC production following coinjection with the RA TNP-OVA. In each case, ASC production was skewed towards the IgG sub(1) isotype. In addition, all three metals induced IgG production to TNP-Ficoll (although relatively weakly in the case of Cd). These results show that each of these metals can provide adjuvant signals to promote lymphocyte proliferation and enhance adaptive immune responses to unrelated antigens. Skewing of immune responses towards T helper type 2 responses suggests that each of these metals can enhance allergic and hypersensitivity reactions to environmental antigens. Furthermore, the induction of IgG responses to TNP-Ficoll, a T-cell-independent antigen, indicates that each of these metals can activate neoantigen-specific T cells. T-cell activation by metals can lead to metal hypersensitivity and has been implicated in the development of autoimmunity. This is the first report of immune modulation by CdCl sub(2) and PbCl sub(2) in the RA-PLNA.

    LA:

    Language
    English

    SL:

    Summary Language
    English

    PY:

    Publication Year
    2006

    PD:

    Publication Date
    200605

    PT:

    Publication Type
    Journal Article

    PB:

    Publisher
    Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP UK, jnl.samples@oup.co.uk, http://www3.oup.co.uk/jnls/

    CL:

    Classification
    X 24222 Analytical procedures

    UD:

    Update
    200604

    SF:

    Subfile
    Toxicology Abstracts

    AN:

    Accession Number
    6753274

    PG:

    Journal Pages
    113-122

    JV:

    Journal Volume
    91

    JI:

    Journal Issue
    1

Field Codes
    The following field codes are found in the records of this database. Here they are listed in alphabetical order by two-letter code. See Field Codes and Search Examples for detailed descriptions and search examples.

    AB = Abstract IS = ISSN
    AF = Author Affiliation LA = Language
    AN = Accession Number NT = Notes
    AU = Authors NU = Other Numbers
    CA = Corporate Author OT = Original Title
    CF = Conference PB = Publisher
    CL = Classification Code PT = Publication Type
    DE = Descriptors PY = Publication Year
    ED = Editor SF = Subfile Name
    EM = Entry Month SL = Summary Language
    ER = Environmental Regime SO = Source
    IB = ISBN TI = Title
    ID = Identifiers TR = ASFA Input Center Number