Disease relevance of Tokunol M

• The upA12 mutation caused twofold resistance to amiprophos-methyl and oryzalin, and twofold hypersensitivity to the microtubule-stabilizing drug taxol, suggesting that the mutation enhanced microtubule stability [1].
• Following 2-year trials, amiprofos-methyl (APM) was found to be superior to oryzalin on the basis of a lower toxicity, and we were able to narrow the range of concentrations of APM [2].

High impact information on Tokunol M

• Depolymerization of microtubules by short treatments with the drug amiprophosmethyl during anaphase and telophase abolished MMK3 activity, indicating that intact microtubules are required for MMK3 activation [3].
• Nuclear fusion in newly formed Chlamydomonas reinhardtii zygotes can be inhibited by drugs that affect microtubule stability, which include colchicine, amiprophosmethyl, oryzalin, and taxol [4].
• The results suggest a common binding site on beta-tubulin for RH-4032, pronamide, zarilamide, and chlorpropham, which is distinct from the binding site(s) for trifluralin and amiprophosmethyl [5].
• Protoplasts treated transiently with the reversible microtubule-disrupting agent amiprophos-methyl (applied before and during centrifugation) elongated but without a preferential growth axis [6].
• Diploids homozygous for mutant alleles of apm1 are 4-6-fold resistant to APM and ORY; diploids homozygous for apm2 are ts- and 2-fold resistant to the herbicides [7].

Biological context of Tokunol M

• Under massive Ca2+-loading conditions amiprophosmethyl inhibited the Ca2+ transport system directly without a significant effect on the respiratory chain, the membrane potential or Ca2+ efflux [8].
• In the next phase of amiprophos-methyl and oryzalin action, however, all non-kinetochore MTs, and especially those most sensitive to these drugs, polar microtubules, which form abundantly during anaphase, disassemble [9].
• A final experiment with 6,658 embryos demonstrated that a 2-day treatment in liquid media supplemented with 50 microM APM was the most successful with respect to chromosome doubling-36.7% of the plants were diploid-but the survival rate was reduced to 52.5% of that of the non-treated control [2].
• Three independent pleiotropic drug-resistance (pdr) mutants were isolated by selecting for resistance to the anti-microtubule herbicides amiprophos-methyl (APM) and oryzalin (ORY) [10].
• Oryzalin and amiprophos-methyl (APM) disrupted microtubules, gravitropism, and normal tip growth and zonation, but did not prevent plastid sedimentation [11].

Anatomical context of Tokunol M

• In maize mitochondria the effect of the herbicide amiprophosmethyl was studied on massive and limited Ca2+-loading and on mitochondrial energy transduction [8].
• Amiprophosmethyl inhibits organelle streaming and collapses the clear zone of vesicles at the extreme tip together with the disruption of microfilaments leading into the tip, leaving the plasma membrane intact [12].
• APM treatments of 30-60 min increased the plastid sedimentation that is normally seen along the length of untreated or control cells [13].
• The roles of cellulose microfibrils and cortical microtubules in establishing and maintaining the pattern of secondary-cell-wall deposition in tracheary elements were investigated with direct dyes to inhibit cellulose microfibril assembly and amiprophosmethyl to inhibit microtubule polymerization [14].

Associations of Tokunol M with other chemical compounds

• The effect of the antimitotic herbicides amiprophosmethyl, trifluralin, and oryzalin upon flagellar regeneration in Chlamydomonas reinhardtii has been studied [15].
• Microtubules (MTs) of cells of Spirogyra sp. were depolymerized by treatment with amiprophos-methyl (APM) for 1 h and then reorganized in 0.30 M mannitol solution [16].
• CYP2B22 rice plants showed tolerance towards 12 herbicides including chlortoluron (100 microM), amiprofos-methyl (2.5 microM), pendimethalin (10 microM), metolachlor (2.5 microM), and esprocarb (20 microM) [17].
• During cycloheximide, but not APM, inhibition cortical microtubules return; however, due to the inhibition of cellulose synthesis itself, they cannot exert their orienting influence [18].

Gene context of Tokunol M

• To determine whether the cytoskeleton restricts plastid sedimentation, the effects of amiprophos-methyl (APM) and cytochalasin D (CD) on plastid position were quantified [13].
• Since APM has been claimed to act selectively on tubulin synthesis in Chlamydomonas it was decided to compare the effects of this compound with cycloheximide (10 microgram/ml) on the recovery of microfibril orientation after colchicine treatment [18].

Analytical, diagnostic and therapeutic context of Tokunol M

• Exposure of the early-log phase suspension culture to 32muM APM led to a marked increase in the MI 12 and 24h after treatment, while higher as well as lower concentrations (16, 24 and 48muM) had no effect [19].

References