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Toxicological information

Specific investigations: other studies

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Administrative data

Endpoint:
biochemical or cellular interactions
Type of information:
experimental study
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Non guideline study. GLP-status unknown. Published in peer reviewed literature. Restrictions in design and reporting but adequate for assessment.

Data source

Reference
Reference Type:
publication
Title:
Pyridine and imidazole reversibly inhibit the respiratory burst in porcine and human neutrophils: Evidence for the involvement of cytochrome b558 in the reaction
Author:
Iizuka T., Kanegasaki S., Makino R., Tanaka T., Ishimura Y.
Year:
1985
Bibliographic source:
Biochemical And Biophysical Research Communications, Vol 130(2), 621-626

Materials and methods

Principles of method if other than guideline:
Porcine and human neutrophils were isolated from peripheral blood. Oxygen consumption was measured spectrophotometrically after addition of the test substance.
GLP compliance:
not specified
Type of method:
in vitro
Endpoint addressed:
other: Respiratory burst

Test material

Constituent 1
Chemical structure
Reference substance name:
2-methylpyridine
EC Number:
203-643-7
EC Name:
2-methylpyridine
Cas Number:
109-06-8
Molecular formula:
C6H7N
IUPAC Name:
2-methylpyridine
Details on test material:
- Name of test material (as cited in study report): 2-methylpyridine

Test animals

Species:
other: Porcine and human neutrophils

Administration / exposure

Details on study design:
Porcine and human neutrophils were isolated from peripheral blood. Oxygen consumption was measured. The cells in Hanks' solution were stimulated by 100 ng/mL of PMA or 2.5 mg/mL of normal-serum opsonized zymosan. Absorption spectrophotometry at 77 K was carried out with spectrophotometer equipped with a low temperature attachment.

Results and discussion

Details on results:
The test substance inhibited the respiratory burst in neutrophils. Inhibition was accompanied by a spectral change in reduced cytochrome B558. Both changes were reversible.
The test substance inhibited the NADPH-dependent oxygen consumption in PMA-stimulated lysed cells. Oxygen consumption in these circumstances was restored by the addition of NADPH.

Applicant's summary and conclusion