Spinosad

Names

[ Name ]:
Spinosad

[Synonym ]:
13-{[5-(Dimethylamino)-6-methyltetrahydro-2H-pyran-2-yl]oxy}-9-ethyl-14-methyl-2-[(2,3,4-trimethoxy-5-methylcyclohexyl)oxy]octadecahydro-1H-as-indaceno[3,2-d]oxacyclododecine-7,15-dione
1H-as-Indaceno[3,2-d]oxacyclododecin-7,15-dione, 13-[[5-(dimethylamino)tetrahydro-6-methyl-2H-pyran-2-yl]oxy]-9-ethyloctadecahydro-14-methyl-2-[(2,3,4-trimethoxy-5-methylcyclohexyl)oxy]-
Spinosyn A

Biological Activity

[Description]:

Spinosad, a mixture of spinosyns A and D known as fermentation products of a soil actinomycete (Saccharopolyspora spinosa), is a biological neurotoxic insecticide with a broader action spectrum. Spinosad targets the nicotinic acetylcholine receptor (nAChRs) of the insect nervous system. Spinosad has an excellent environmental and mammalian toxicological profile. Larvicidal activity[1][2][3].

[Related Catalog]:

Signaling Pathways >> Membrane Transporter/Ion Channel >> nAChR

Signaling Pathways >> Neuronal Signaling >> nAChR

Research Areas >> Neurological Disease

[In Vitro]

Spinosad acts as an allosteric agonist of acetylcholine (Ach) by binding to nicotinicacetylcholine receptors (nAChRs), prototypicalunits that function as neurotransmitter ligand-gated ion channels[4].

[In Vivo]

Spinosad is a natural mixture of the pediculicidal tetracyclic macrolides spinosyn A and spinosyn D. Spinosad 0.9% mainly interferes with nicotinic acetylcholine receptors in insects, thereby producing neuronal excitation that results in paralysis of lice from neuromuscular fatigue after extended periods of hyperexcitation. Spinosad 0.9% kills both permethrin-susceptible and permethrin-resistant populations of lice. It is also ovicidal, killing both eggs (nits) and lice[5]. Spinosad causes in vivo oxidative effects in the brain of Oreochromis niloticus. Spinosad causes elevations in the contents of tGSH, GSH, GSSG, Hsp70, and reductions in the ratio of GSH/GSSG and GPx activity and an induction in the GR (glutathione reducta) activity. Spinosad has oxidative effects in the brain tissue by altering the parameters in GSH-related antioxidant system and Hsp70[6].

[References]

[1]. Duchet C, et al. Effects of Bacillus thuringiensis israelensis and spinosad on adult emergence of the non-biting midges Polypedilum nubifer (Skuse) and Tanytarsus curticornis Kieffer (Diptera: Chironomidae) in coastal wetlands. Ecotoxicol Environ Saf. 2015;115:272-278.

[2]. Wang J, et al. A three amino acid deletion in the transmembrane domain of the nicotinic acetylcholine receptor α6 subunit confers high-level resistance to spinosad in Plutella xylostella. Insect Biochem Mol Biol. 2016;71:29-36.

[3]. Huang J, et al. High Level of Spinosad Production in the Heterologous Host Saccharopolyspora erythraea. Appl Environ Microbiol. 2016;82(18):5603-5611. Published 2016 Aug 30.

[4]. McCormack PL. Spinosad: in pediculosis capitis. Am J Clin Dermatol. 2011;12(5):349-353.

[5]. Santos VSV, et al. Properties, toxicity and current applications of the biolarvicide spinosad. J Toxicol Environ Health B Crit Rev. 2020;23(1):13-26.

[6]. Piner P, et al. Organic insecticide spinosad causes in vivo oxidative effects in the brain of Oreochromis niloticus. Environ Toxicol. 2014;29(3):253-260.