<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml"><p>Strategies for the use of bio-indicators in the prediction of environmental damage should include mechanistic research. This study involves the relationship between the chemical structure and hemotoxic markers of aniline and its halogenated analogs. Aniline-induced methemoglobinemia, loss of circulating blood cells, blood stability, glutathione depletion and membrane cytoskeletal changes were assessed following exposure to phenylhydroxylamine (PHA), <italic>para</italic>-fluoro-, <italic>para</italic>-bromo-, and <italic>para</italic>-iodo in male Sprague-Dawley rats. Methemoglobin was determined spectrophotometrically at 635 nm. Erythrocyte depletion was investigated by loss of radioactivity in chromium-labeled red blood cells <italic>in vivo.</italic> Membrane proteins were analyzed by SDS-PAGE using red blood ghost cells treated with various aniline analogs. Results showed dose- and time-dependent changes in the induction of methemoglobin of up to 78 % with <italic>para</italic>-bromo PHA and 75 % with <italic>para</italic>-iodo PHA compared to 3 % to 5 % in control. Treated animals lost up to three times more blood from circulation compared to control within 14 days after treatment. Erythrocytes were more stable in buffer solution than in <italic>para</italic>-iodo-treated cells. Depletion of reduced glutathione in PHA and <italic>para</italic>-iodo-PHA treated red cells was also observed. Analysis of red cell skeletal membrane treated with <italic>para</italic>-iodo-PHA showed that protein band 2.1 became broader and band 2.2 diminished completely in some treatments. Dose- and time-dependent changes suggested the use of hemotoxic endpoints as potential biomarkers for assessing chemical and drug safety.</p></abstract>

Strategies for the use of bio-indicators in the prediction of environmental damage should include mechanistic research. This study involves the relationship between the chemical structure and hemotoxic markers of aniline and its halogenated analogs. Aniline-induced methemoglobinemia, loss of circulating blood cells, blood stability, glutathione depletion and membrane cytoskeletal changes were assessed following exposure to phenylhydroxylamine (PHA), para-fluoro-, para-bromo-, and para-iodo in male Sprague-Dawley rats. Methemoglobin was determined spectrophotometrically at 635 nm. Erythrocyte depletion was investigated by loss of radioactivity in chromium-labeled red blood cells in vivo. Membrane proteins were analyzed by SDS-PAGE using red blood ghost cells treated with various aniline analogs. Results showed dose- and time-dependent changes in the induction of methemoglobin of up to 78 % with para-bromo PHA and 75 % with para-iodo PHA compared to 3 % to 5 % in control. Treated animals lost up to three times more blood from circulation compared to control within 14 days after treatment. Erythrocytes were more stable in buffer solution than in para-iodo-treated cells. Depletion of reduced glutathione in PHA and para-iodo-PHA treated red cells was also observed. Analysis of red cell skeletal membrane treated with para-iodo-PHA showed that protein band 2.1 became broader and band 2.2 diminished completely in some treatments. Dose- and time-dependent changes suggested the use of hemotoxic endpoints as potential biomarkers for assessing chemical and drug safety.

Mechanistic Study on Aniline-Induced Erythrocyte Toxicity

Department of Natural Science and Mathematics, College of Sciences and Technology, Savannah State University, Savannah, Georgia, USA

Archives of Industrial Hygiene and Toxicology

{"article-title":"Mechanistic Study on Aniline-Induced Erythrocyte Toxicity"}

Strategies for the use of bio-indicators in the prediction of environmental damage should include mechanistic research. This study involves the relationship...

Mechanistic Study on Aniline-Induced Erythrocyte Toxicity

Data publikacji: 03 paź 2007

Zakres stron: 275 - 285

DOI: https://doi.org/10.2478/v10004-007-0018-2

Słowa kluczowe
bjelančevine citoskeleta, hemolitička anemija, hemotoksičnost, fenilhidroksilamin, methemoglobin, -bromofenilhidroksilamin, -fluorofenilhidroksilamin, -jodofenilhidroksilamin

This content is open access.

Mechanistic Study on Aniline-Induced Erythrocyte Toxicity

Data publikacji: 03 paź 2007

Zakres stron: 275 - 285

DOI: https://doi.org/10.2478/v10004-007-0018-2

Słowa kluczowebjelančevine citoskeleta, hemolitička anemija, hemotoksičnost, fenilhidroksilamin, methemoglobin, -bromofenilhidroksilamin, -fluorofenilhidroksilamin, -jodofenilhidroksilamin

This content is open access.

Słowa kluczowe
bjelančevine citoskeleta, hemolitička anemija, hemotoksičnost, fenilhidroksilamin, methemoglobin, -bromofenilhidroksilamin, -fluorofenilhidroksilamin, -jodofenilhidroksilamin