Mode of Actionc

Relative Toxicity

Inhibitor of acetyl coenzyme-A carboxylase (ACCase), a pivotal enzyme in plant fatty acid biosynthesis.

Varies based on specific chemical compound; likely to be carcinogenic to humans according to EPA Proposed EPA Weight-of-the-Evidence Categories (US-EPA, 2009a).

Inhibition of cell division (long-chain fatty acid inhibitor).

Slightly toxic; oral RfD* of 1 × 102 mg/kg-day. Critical effects: hemosiderosis, hemolytic anemia (US-EPA, 2009b).

Inhibition of the acetolactate synthase (ALS) enzyme resulting in cessation of the biosynthesis of essential branched chain amino acids (leucine, valine, and isoleucine).

Varied; generally low acute and chronic toxicity to humans and not likely to be carcinogenic.

Inhibit photosynthesis by binding with a specific protein in the photosystem II complex.

Slightly to moderately toxic; oral RfD of 3.5 × 102 mg/kg-day. Critical effects: decreased body weight gain (other effect: cardiac toxicity and moderate-to-severe dilation of the right atrium (EXTOXNET, 2009a; US-EPA, 2009c)).

The specific mode of action is not well defined, however these herbicides mimic the endogenous auxin indoleacetic acid, a plant hormone that stimulates growth and appears to negatively affect cell wall plasticity and nucleic acid metabolism.

Relatively nontoxic. Acute oral LD50 in rats is 1707 mg/kg, dermal LC50§ in rabbits is >2000 mg/kg. However, eye irritation in rabbit is extreme.

Inhibits the activity of glutamine synthetase, which causes ammonia buildup in the cell. The ammonia destroys cell membranes.

Practically nontoxic by ingestion; some increase in absolute and relative kidney weights in males. No observed carcinogenesis. Oral RfD of 4 × 104 mg/kg-day (NPIC, 2009; US-EPA, 2009d).

Inhibits the EPSP synthase, which leads to depletion of essential aromatic amino acids (tryptophan, tyrosine, and phenylalanine).

Generally nontoxic. Increased incidence of renal tubular dilation in third generation weanlings. Oral RfD of 1 × 101 mg/kg-day (US-EPA, 2009e).

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