6533b7d7fe1ef96bd1267b0f

RESEARCH PRODUCT

Immunoreactivity of Roach,Rutilus rutilus,Following Laboratory Exposure to Bleached Pulp and Paper Mill Effluents

T.m. AaltonenE.i. JokinenE. T. Valtonen

subject

PaperBleachHealth Toxicology and MutagenesisCyprinidaeImmunoglobulinsIndustrial Wastechemistry.chemical_elementengineering.materialchemistry.chemical_compoundImmune ToleranceChlorineCyprinidaeAnimalsFood scienceChlorine dioxidebiologybusiness.industryEcologyPulp (paper)Public Health Environmental and Occupational HealthOxidesPaper millGeneral Medicinebiology.organism_classificationPollutionchemistryToxicityengineeringChlorineRutilusChlorine CompoundsbusinessSpleenWater Pollutants ChemicalDisinfectants

description

Abstract In order to study immunomodulation, controlled laboratory experiments were carried out with roach ( Rutilus rutilus ) exposed to bleached kraft mill effluent (BKME) or spent bleach liquor (SBL) from two pulp and paper mills using elementary chlorine and chlorine dioxide for bleaching. The total number of immunoglobulin-secreting cells (ISC) and the number of specific antibody-secreting cells (ASC) were determined by ELISPOT assay. Exposure to BKME resulted in decreased numbers of ISC in the spleen. To study the capability of response against foreign antigens the fish were immunized with bovine γ-globulin. Exposure to BKME or SBL reduced antigen-specific ASC response in fish. Moreover, the suppression of ASC response did not require exposure prior to immunization. Depuration of fish in clean water reveals that the immunosuppression caused by BKME is reversible. The ASC response in the BKME-pretreated fish returned to the same or even a higher level compared to untreated immunized fish and, in addition, the number of ISC increased greatly. The results of this study verify an earlier finding on poor antibody response due to exposure in a lake contaminated with BKME. Exposure to SBL alone suppresses antibody-mediated immunity, suggesting that compounds formed in bleaching are at least partly responsible for immunotoxic effects.

https://doi.org/10.1006/eesa.1997.1588