Agronomy for Sustainable Development, An International Journal in Agriculture and Environment

Momilactones A (M_A) and B (M_B) are phytoalexins derived from rice plant (Oryza sativa) and were considered to be a part of the mechanism of rice self-defense system. The present study was to evaluate the comparative efficacies in vitro of antibacterial, fungicidal, antioxidant, and herbicidal activities of M_A and M_B. In general, M_B shows higher antifungal, antibacterial, and herbicidal action than M_A, although its antioxidant property was less than M_A. In herbicidal trial, the IC₅₀ values of M_B against germination, shoot and root elongation of barnyardgrass and monochoria were 40.9, 45.5, and 27.5, and 27.1, 17.3, and 0.9 µg, respectively. For M_A, these values were 40.3, 35.6, and 55.1, and 43.9, 24.3, and 0.5 µg, respectively. For antifungal activity, momilactone B (IC₅₀: 1.2, 123.9, and 53.4 µg) exerted significantly greater inhibition than M_A (IC₅₀: 78.1, 198.1, and 95.3 µg) against Botrytis cinerea, Fusarium solani, Colletrotrichum gloeosporioides, respectively, except for Fusarium oxysporum that both M_A and M_B showed no marked difference. In addition, M_B exhibited significantly stronger antibacterial activity than M_A against Pseudomonus ovalis, Bacillus cereus, and Bacillus pumilus, whereas the inhibitory activity of the two compounds was similar against Escherichia coli. Both M_A and M_B exerted rather weak antioxidant activity (EC₅₀ was 783.9 and 790.7 µg, respectively), of which M_A showed a slightly stronger antioxidant activity than M_B. This study is the first to examine antifungal, antibacterial, and antioxidant activities of two phytoalexins, as well as their comparative efficacies against growth of the noxious weeds barnyardgrass and monochoria.

Background: Anoctamin 1 (ANO1 or TMEM16A) Ca²⁺-gated Cl⁻ channels of nociceptor neurons are emerging as important molecular components of peripheral pain transduction. At physiological intracellular Cl⁻ concentrations ([Cl⁻]_i) sensory neuronal Cl⁻ channels are excitatory. The ability of sensory neuronal ANO1 to trigger action potentials and subsequent nocifensive (pain) responses were examined by direct activation with an N-aroylaminothiazole. ANO1 channels are also activated by intracellular Ca²⁺ ([Ca²⁺]_i) from sensory neuronal TRPV1 (transient-receptor-potential vallinoid 1) ion channels and other noxicant receptors. Thus, sensory neuronal ANO1 can facilitate TRPV1 triggering of action potentials, resulting in enhanced nociception. This was investigated by reducing ANO1 facilitation of TRPV1 effects with: (1) T16A[inh]-A01 ANO1-inhibitor reagent at physiological [Cl⁻]_i and (2) by lowering sensory neuronal [Cl⁻]_i to switch ANO1 to be inhibitory. Results: ANO1 effects on action potential firing of mouse dorsal root ganglia (DRG) neurons in vitro and mouse nocifensive behaviors in vivo were examined with an N-aroylaminothiazole ANO1-activator (E-act), a TRPV1-activator (capsaicin) and an ANO1-inhibitor (T16A[inh]-A01). At physiological [Cl⁻]_i (40 mM), E-act (10 μM) increased current sizes (in voltage-clamp) and action potential firing (in current-clamp) recorded in DRG neurons using whole-cell electrophysiology. To not disrupt TRPV1 carried-Ca²⁺ activation of ANO1 in DRG neurons, ANO1 modulation of capsaicin-induced action potentials was measured by perforated-patch (Amphotericin–B) current-clamp technique. Subsequently, at physiological [Cl⁻]_i, capsaicin (15 μM)-induced action potential firing was diminished by co-application with T16A[inh]-A01 (20 μM). Under conditions of low [Cl⁻]_i (10 mM), ANO1 actions were reversed. Specifically, E-act did not trigger action potentials; however, capsaicin-induced action potential firing was inhibited by co-application of E-act, but was unaffected by co-application of T16A[inh]-A01. Nocifensive responses of mice hind paws were dramatically induced by subcutaneous injections of E-act (5 mM) or capsaicin (50 μM). The nocifensive responses were attenuated by co-injection with T16A[inh]-A01 (1.3 mM). Conclusions: An ANO1-activator (E-act) induced [Cl⁻]_i-dependent sensory neuronal action potentials and mouse nocifensive behaviors; thus, direct ANO1 activation can induce pain perception. ANO1-inhibition attenuated capsaicin-triggering of action potentials and capsaicin-induced nocifensive behaviors. These results indicate ANO1 channels are involved with TRPV1 actions in sensory neurons and inhibition of ANO1 could be a novel means of inducing analgesia.