Upregulation of Metabolic Defense System After Short-term Exposure to Formulated Insecticide

The rising use of formulated insecticides called for an evaluation of their effects on the substantia nigra defensive mechanisms to identify potential therapeutic windows.

The purpose of this study is to assess the defense system of substantia nigra after shortterm exposure to formulated pyrethroid insecticide.

A total of 32 adult Wistar rats were randomly assigned to 4 groups, each consisting of 8 animals. Group A was kept as the control group, while groups B, C, and D were given a mixture of dichlorvos and cypermethrin for 2 h, 3 h, and 4 h/d, respectively, for 4 weeks. The neurobehavioral test was carried out on the final day of exposure. The animals were sacrificed and cardiac perfused with heparinized saline 24 h after the last exposure. An occipitofrontal incision was made to remove the brain to assess glucose and astrocytes. After the brain mapping, the fixation was performed in 10% neutral buffered formalin for 48 h.

Groups A, B, C, and D had glucose levels of 68.91, 71.66, 74.27, and 75.85 mg/dL, respectively, and all of them were statistically significant at P=0.000. The astrocyte expressions were 19.50, 31.13, 33.63, and 57.88 μg/mL in groups A, B, C, and D, respectively, and groups C and D were statistically significant at P=0.026 and P=0.000, respectively, while group B was not significant at P=0.086. The means of motor function were 1.42, 1.33, 1.10, and 0.75 minutes in groups A, B, C, and D, respectively, and the groups B, C, and D were not statistically significant at P=0.999, P=0.936, and P=0.850, respectively.

Regarding the blood-brain barrier and the gliosis process, the structural integrity of astrocytes serves as the first line of protection against xenobiotic (foreign substance) inversion of the brain. According to this research, the increased astrocyte expression and elevated glucose levels are attempts to maintain motor capabilities after exposure to insecticides with pyrethrin formulations, which explains the time-dependent slow decline in the motor activities of the experimental animals.