Naphthalene-1,8-dicarboximide

Additional toxicological data

Administrative data

Endpoint:

additional toxicological information

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: Acceptable, well documented publication which meets basic scientific principles.

Data source

Reference

Reference Type:

publication

Title:

Differential Induction of Cytochrome P450-Mediated Triasulfuron Metabolism by Naphthalic Anhydride and Triasulfuron

Author:

Persans, M.W. and Schuler, M.A.

Year:

1995

Bibliographic source:

Plant Physiol., 109, 1483 - 1490

Materials and methods

Type of study / information:

Biochemical analysis of triasulfuron metabolism in maize (Zea mays) seedlings has demonstrated that the P450(s) responsible for detoxification of this herbicide is induced by naphthalic anhydride (NA), a plant safener, and by triasulfuron, the herbicide itself. Additionally, the induction of triasulfuron metabolism by other naphthalene derivatives, like 1,8-Naphthalimide (NI) was tested.

Test guideline

Qualifier:

no guideline available

Principles of method if other than guideline:

To determine the level of synergistic interaction among safeners, herbicides, and developmental parameters, the level of triasulfuron metabolism in response to NA, some of its structural analogs, like NI, and triasulfuron itself were characterized during different stages in maize (Zea mays) seedling development.

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

1,8-Naphthalimide (NI)

IUPAC Name:

1,8-Naphthalimide (NI)

Details on test material:

No further details.

Results and discussion

Any other information on results incl. tables

Biochemical analysis of triasulfuron metabolism in maize (Zea mays) seedlings has demonstrated that the P450(s) responsible for detoxification of this herbicide is induced by naphthalic anhydride (NA), a plant safener, and by triasulfuron, the herbicide itself. Induction studies of different ages suggest that two separate response pathways modulate this P-450 activity. Induction by NA is independent of the developmental age of the seedlings up to 6.5 d; induction by triasulfuron is tightly modulated with respect to developmental age in that triasulfuron metabolism can be induced by triasulfuron in young (2.5 d) but not older (6.5 d) seedlings. lnduction by NA administered in combination with triasulfuron synergistically enhances triasulfuron metabolism in younger seedlings to levels substantially above that obtained with either herbicide or safener treatment alone. In older seedlings, NA plus triasulfuron treatment induces triasulfuron metabolism to only the level of NA treatment alone, indicating again that the induction cascade responding to triasulfuron is nonfunctional in later development. MnCl₂ studies indicate that the triasulfuron insensitivity of older seedlings does not result from a general limitation in the inducibility of this P-450 detoxification system but rather from specific limitations in the triasulfuron-response pathway. The range of naphthalene derivatives that are capable of inducing triasulfuron metabolism is extremely limited. In combination with triasulfuron treatment, the rank order of the derivatives that were tested as inducers is NA > NDA (2,3-Naphthalene dicarboxylic acid) >> NI = NDiA (1,4,5,8-Naphthalenetetracarboxylic dianhydride). The auxin analog NAA (1-Naphthalene acetic acid) only marginally increases triasulfuron metabolism, and naphthalene itself fails to induce metabolism of this herbicide.