Genotoxic effects of chlorophenoxy herbicide diclofop-methyl in micein vivoand in human lymphocytesin vitro

Abstract

Diclofop-methyl (DM) is a chlorophenoxy derivative used in large quantities for the control of annual grasses in grain and vegetable crops. In this study, the genotoxic effects of DM were investigated by measuring chromosomal aberrations (CAs) in mouse bone-marrow cells and CA and the comet assay in human peripheral lymphocytes. Mice were treated with 15.63, 31.25, 62.5, and 125 mg/kg body weight of DM intraperitoneally for 24 hours, and 15.63-, 31.25-, 62.5-, 125-, and 250-µg/mL concentrations were applied to human lymphocytes for both 24 and 48 hours. In in vivo treatments, DM significantly, but not dose dependently, increased the total chromosome aberrations, compared to both negative and solvent controls. Cell proliferation was significantly, but not dose dependently, affected by all doses. In in vitro treatments, DM (except 15.63 µg/mL) significantly and dose dependently increased the frequency of chromosome aberrations. Also, 250 µg/mL of 48-hour treatment was found to be toxic. Cell proliferation was significantly and dose dependently affected by DM applications, when compared to negative control. In in vitro treatments, DM significantly decreased the mitotic index only at the highest concentration for 24 hours, and 62.5- and 125-µg/mL concentrations for 48 hours. In the comet assay, a significant and dose-dependent increase in comet-tail intensity was observed at 62.5-, 125-, and 250-µg/mL concentrations. The mean comet-tail length was significantly increased in all concentrations. Our results demonstrate that DM is genotoxic in mammalian cells in vivo and in vitro.

Diclofop-methyl: A phenoxy propionate herbicide with multiple toxic effects in mouse embyro fibroblast (NIH/3T3) cell line

“…In positive control (100 μM H 2 O 2 ), the tail intensity was ranged from 55.25-56.96%. Similar to our data, Unal et al [3] found diclofop-methyl was a cyto-and genotoxic agent in human lymphocytes and mouse bone-marrow cells. They observed that a high degree of DNA damage was in lymphocytes from 6.00 ±0.75 to 12.79 ±1.22, respectively.…”

“…Aryloxy phenoxy propionic acid herbicides are one of the major pesticide groups. Diclofop-methyl is a selective, post emergence aryloxy phenoxy propionic acid herbicide primarily used to control wild oat (Avena fatua L.) and other annual graminaceous weeds in wheat, barley, and soybeans [3,17]. Exposure to some of these pesticides may lead to modifications in the genetic material thereby causing mutagenicity, carcinogenicity, teratogenicity and immunotoxicity [16].…”

“…Exposure to some of these pesticides may lead to modifications in the genetic material thereby causing mutagenicity, carcinogenicity, teratogenicity and immunotoxicity [16]. As it is well known, genotoxic potential of pesticides is a risk factor for longterm effects with carcinogenic and reproductive toxicity [3,18]. Department of National Health and Welfare conducted a two-year mouse feeding/oncogenicity study [19].…”

“…Herbicides are widely used, and have an intensive biological effects on pests [3]. Diclofob-methyl, a member of aryloxyphenoxy propanoate herbicide group, inhibits acetyl-CoA carboxylase (ACCase) which is a key enzyme in long-chain fatty acid biosynthesis [4].…”

Cypermethrin and chlorpyrifos raises serum urea level and causes abnormal sperm morphology in Wistar rats

“…CPF can induce toxicity and oxidative stress [22,23]. Experimental data revealed that pesticides such as cypermethrin may possess genotoxic, mutagenic, teratogenic, and carcinogenic properties, inducing mutations, chromosomal alterations, or DNA damage [24]. The prolonged and indiscriminate use of cypermethrin was reported to cause both acute and chronic toxicity in non-target species including humans [25].…”