Protective effect of (−)-α-bisabolol on rotenone-induced toxicity in Drosophila melanogaster

Author:

Leite Gerlânia de Oliveira1,Ecker Assis2,Seeger Rodrigo Lopes2,Krum Bárbara Nunes2,Lugokenski Thiago Henrique3,Fachinetto Roselei1,Sudati Jéssie Haigert3,Barbosa Nilda Vargas2,Wagner Caroline13

Affiliation:

1. Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, Santa Maria – RS, Brazil.

2. Programa de Pós-Graduação em Ciências Biológicas – Bioquímica Toxicológica, Universidade Federal de Santa Maria, Santa Maria – RS, Brazil.

3. Universidade Federal do Pampa, Campus Caçapava do Sul, Caçapava do Sul – RS, Brazil.

Abstract

(−)-α-Bisabolol (BISA) is a sesquiterpene alcohol, which has several recognized biological activities, including anti-inflammatory, anti-irritant, and antibacterial properties. In the present study, we investigated the influence of BISA (5, 25, and 250 μmol/L) on rotenone (500 μmol/L)-induced toxicity in Drosophila melanogaster for 7 days. BISA supplementation significantly decreased rotenone-induced mortality and locomotor deficits. The loss of motor function induced by rotenone correlated with a significant change in stress response factors; it decreased thiol levels, inhibited mitochondria complex I, and increased the mRNA expression of antioxidant marker proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product. Taken together, our findings indicate that the toxicity of rotenone is likely due to the direct inhibition of complex I activity, resulting in a high level of oxidative stress. Dietary supplementation with BISA affected the expression of SOD mRNA only at a concentration of 250 μmol/L, and did not affect any other parameter measured. Our results showed a protective effect of BISA on rotenone-induced mortality and locomotor deficits in Drosophila; this effect did not correlate with mitochondrial complex I activity, but may be related to the antioxidant protection afforded by eliminating superoxide generated as a result of rotenone-induced mitochondrial dysfunction.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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