of molecules in the chloroplast, causing substantial damage to photosynthetic activity [39]. Phytotoxicity
is associated with quaternary nitrogen salts in which the nitrogens are in positions 2,2 -, 2,4 -, and 4,4 -.
Maximum herbicide activity is produced when the two rings of pyridine adopt a planar configuration. The
two most important herbicides of the bipyridilium family are diquat (2,2 -bipyridyl) and paraquat, also
known as methyl viologen (4,4 -bipyridyl), the latter being used more. These herbicides inhibit cyclic as
well as noncyclic phosphorylation and the reduction of NADPeven upon the addition of ascorbate plus
DPIP [4,12,40].
These herbicides are absorbed through the leaves. They are not selective and they do not present
residual activity in soil because they quickly adhere to the colloids of the soil. Paraquat is more active on
monocotyledons, diquat on dicotyledons.
In our laboratory, the action of methyl viologen was used in artificial photosystems for the produc-
tion of hydrogen peroxide by free and immobilized microalgae and chloroplasts. Methyl viologen acting
on PSI is reduced by electron flow and reoxidized by oxygen, producing O 2 , with a concurrent increase
of hydrogen peroxide present in the system [39]. Hydrogen peroxide is an energetic compound that can
be used as engine and rocket fuel [41–45].
RESISTANCE There are no known species of paraquat-resistant annual crops. About 18 species of
weeds have been found with resistance, but the resistance mechanisms are not clearly understood [1,46].
A plant having the capacity to metabolize these herbicides has not been found in susceptible species or in
evolved resistant biotypes [47,48]. Resistance can be conferred by increasing the ability to eliminate the
toxic species of oxygen; thus, O 2 can be converted to hydrogen peroxide by superoxide dismutase and
hydrogen peroxide decomposed to oxygen and water by catalase. Other enzymes, such as ascorbate per-
oxidase and glutathione reductase, can produce detoxification of the active oxygen species. Higher activ-
ity of these enzymes has been found in crude leaf extracts and chloroplasts [49–52]. Therefore, the in-
creasing activity of the enzymes in transgenic plants should enable the use of paraquat in a more profitable
way [53,54]. Probably another resistance mechanism involves restriction of the mobility of these herbi-
cides, but no evidence has been found for a molecular mechanism restricting mobility or site of compart-
mentalization.
III. AMINO ACID SYNTHESIS INHIBITORS
Among herbicides included in this group are sulfonylureas, imidazolinones, sulfonamides, isopropy-
lamines, and some substituted amino acids. These chemicals inhibit enzymes that participate in the syn-
thesis of the amino acids necessary for normal development and plant growth.
A. ALS Inhibitors
Sulfonylureas, imidazolinones, and sulfonamides act on the enzyme acetolactate synthetase (ALS). This
enzyme catalyzes the first reaction of the metabolic pathway that synthesizes isoleucine, leucine, and va-
line (Figure 3). It has been shown that these herbicides inhibit specifically and potentially the ALS of
plants and bacteria in vitro [55–57].
The ALS inhibitors are absorbed by leaves and by roots, moving easily via the phloem as well as the
xylem to the growing zones. These herbicides affect the leaves of both annual and perennial plants.
RESISTANCE In crops, resistance to this type of herbicide is based on the capacity for metabolic in-
activation rather than on a difference in herbicide uptake or on modification of the affinity of ALS
[58–60]. For example, wheat and corn produce hydroxylation followed by conjugation of substituted sul-
fonylurea [61,62]. Genetic engineering has been used to produce transgenic species with less susceptible
ALS. Genes from resistant mutants have been introduced into tobacco by transformation and have con-
ferred useful levels of herbicide resistance in transgenic plants [63,64].
Multiple resistance forms have emerged in weeds because of the extended use of sulfonylureas.
Many species of Lolium,Lactuca,Salsola, etc. have evolved resistance to ALS inhibitors in different
countries [65–67]. The resistance in these cases is based fundamentally on metabolic inactivation rather
than on a less susceptible ALS [68]. The resistance appears to be a quantitative (polygenic) characteris-
tic, although in some cases, such as in Lactucaspp., a single mutation in ALS prevents its recognition by
inhibitors [69].
778 DE LA ROSA