Effect of organic tomato ( Lycopersicon esculentum ) extract on the genotoxicity of doxorubicin in the Drosophila wing spot test

Abstract

The consumption of organic tomatoes (ORTs) reduces the risk of harmful effects to humans and the environment caused by exposure to toxic agrochemicals. In this study, we used the somatic mutation and recombination test (SMART) of wing spots in Drosophila melanogaster to evaluate the genotoxicity of ORT and the effect of cotreatment with ORT on the genotoxicity of Doxorubicin® (DXR, a cancer chemotherapeutic agent) that is mediated by free radical formation. Standard (ST) cross larvae were treated chronically with solutions containing 25%, 50% or 100% of an aqueous extract of ORT, in the absence and presence of DXR (0.125 mg/mL), and the number of mutant spots on the wings of emergent flies was counted. ORT alone was not genotoxic but enhanced the toxicity of DXR when administered concomitantly with DXR. The ORT-enhanced frequency of spots induced by DXR may have resulted from the interaction of ORT with the enzymatic systems that catalyze the metabolic detoxification of this drug.

Anti/genotoxic, longevity inductive, cytotoxic, and clastogenic‐related bioactivities of tomato and lycopene

“…The DNA stability or lack of genotoxicity observed for all concentrations of tomato and lycopene confirm that they are safe to be consumed. These results agree with those obtained by Dutra et al [] with aqueous organic tomato extract at higher concentrations than ours (1 g/mL) in the same in vivo genetic model. Studies with mice have also demonstrated the safe use of tomato paste and tomato juice using micronucleus test [Velmurugan et al, ; Asita et al, ].…”

“…This fruit contains many bioactive molecules, including those that act as antioxidants, such as ascorbic acid, vitamin E, carotenoids, flavonoids, and phenolic acid [Toor and Savage, ] and for this reason the status of functional food due to the association between its consumption and a reduced risk of certain types of cancers and cardiovascular diseases has been assumed for tomato [Willcox et al, ; Canene‐Adams et al, ; Silaste et al, ; Palozza et al, ]. It is not genotoxic in Drosophila [Dutra et al, ], reduces the mutagenicity induced by aflatoxin B1 (AFB1), benzo[a] pyreno (BaP), cyclophosphamide (CP), and 2‐amino‐3‐methylimidazo [4,5‐f] quinolone (IQ) in Salmonella typhimurium [Rauscher et al, ; Rodríguez‐Muñoz et al, ], protects against 7,12 dimethylbenz[a]anthracene (DMBA) and N ‐methyl‐ N ‐nitro‐ N ‐nitrosoguanidine (MNNG)‐induced genetic damage in mice [Bhuvaneswari et al, ; Velmurugan et al, ], has an anticarcinogenic effect in Swiss albino and C57 Bl mice [Agrawal et al, ] and is cytotoxic in different cancer cell lines [Friedman et al, ].…”

Mikania glomerataSprengel (Asteraceae) Influences the Mutagenicity Induced by Doxorubicin without Altering Liver Lipid Peroxidation or Antioxidant Levels

“…Other studies also demonstrated an interaction of different agents, including secondary metabolites and crude extracts of plants, resulting in enhanced risk for genotoxicity (Ansah et al 2005;Araújo et al 1998), similar to the organic tomato extract that enhanced genotoxicity induced by DXR in the Drosophila wing spot test (Dutra et al 2009). …”

Vernonanthura polyanthes leaves aqueous extract enhances doxorubicin genotoxicity in somatic cells of Drosophila melanogaster and presents no antifungal activity against Candida spp.

“…When (-)-cubebin, a compound isolated from Piper cubeba seeds, was combined with DXR, the number of mutant spots increased (Rezende et al, 2011). The extract of organic tomato Lycopersicon esculentum when combined with DXR also potentiates the genotoxic effect of this drug (Dutra et al, 2009). T. impetiginosa alone did not act as a genotoxin or an antigenotoxin, but it induced the DXR genotoxicity when associated with this mutagen (Sousa et al, 2009).…”

“…But the components and mechanisms used by some plants to enhance DXR genotoxic effect were not revealed yet. DXR is a chemotherapeutic agent that induces single-and double-stranded DNA breaks (Rezende et al, 2011), after being metabolized by cytochrome P450 complex (Dutra et al, 2009). Interestingly, this enzyme complex is also responsible for DXR detoxification (Niitsu et al, 2000).…”