Carotenoid Biosynthesis Inhibitors

These herbicides applied as preemergence or postemergence in different cropping systems, landscape and ornamental, industrial use, and aquatic setting. In general, they are active on broadleaf weeds but control selected grasses. The Carotenoid Biosynthesis Inhibiting herbicides interfere directly or indirectly with carotenoid production that protects chlorophyll from excessive light and photo oxidation.

Ultimately, chlorophyll production is inhibited, and plant foliage turns white and appears bleached. Although injury symptoms are similar with these herbicides; the specific site of action is different. The Carotenoid Biosynthesis Inhibitors are classified in three subgroups based on modes of action. These groups are:

Inhibition of carotenoid biosynthesis at the phytoene desaturase step (PDS)

HRAC Group: F1

WSSA Group: 12

Pyridiazinones herbicides are examples of the group that block carotenoid biosynthesis by inhibition of phytoene desaturase a key enzyme in carotenoid biosynthesis pathway. Carotenoids are largely absent when plants treated with these herbicides allowing destruction of membrane fatty acid, chlorophyll by excessive energy.

Inhibition of 4-hydroxyphenyl-pyruvate-dioxygenase (HPPD)

HRAC Group: F2

WSSA Group: 27

Callistemones, isoxazoles, and triketones are examples of herbicides that inhibit phydroxyphenyl pyruvate dioxygenase (HPPD). This enzyme catalyzes a key step in plastoquinone biosynthesis and its inhibition gives rise to bleaching symptoms. These symptoms result from an indirect inhibition of carotenoid synthesis due to the involvement of plastoquinone as a cofactor of phytoene desaturase.

Inhibition of carotenoid biosynthesis (unknown target)

HRAC Group: F3

WSSA Group: 11, 13

The isoxazolidinone herbicide clomazone and the triazole herbicide amitrol are examples of this group. The modes of action of these herbicides are not clearly illustrated. Recent evidence, however, suggests that clomazone is metabolized to another form of clomazone, which is herbicidal active and inhibits 1-deoxy-D-xyulose 5-phosphate synthase (DOXP), a key component to plastid isoprenoid synthesis. Amitrole inhibits accumulation of chlorophyll and carotenoids in the light, although the specific site of action has not been determined.

Injury symptoms: Injury symptoms from the carotenoid biosynthesis herbicides are expressed as white to translucent foliage. Plant foliage appears beached and sometimes with purpling of the leaf margins. In trees and woody ornamentals, symptoms may appear as veinal chlorosis or bleaching. In carotenoid biosynthesis herbicide drift cases bleaching and slight chlorosis may develop within 72 hours of exposure depending on rates and plant species, followed by necrosis in the most severe cases. Leaves that develop after exposure may be crinkled and distorted. Three to four weeks after exposure, plants may recover and appear normal.

Chemistry Group and Common Names of CB Inhibitors
Used in the United States