(A) Cysteinyl-dopamine levels were below the detection limit (BDL) in control and 1 mg/kg animals but present in highest dose group. Cysteinyl-DOPAC levels were increased by 85% and 241% in the striatum of mice dosed with 1 mg/kg and 3 mg/kg dieldrin, respectively (*p<0.05, ***p<0.001; overall p<0.0001). Mean values ± SEM for cys-DA levels was 0.165 ± 0.061 pmol/mg tissue for the 3mg/kg group. Mean values ± SEM for cys-DOPAC levels were 0.100 ± 0.014, 0.185 ± 0.025, and 0.341 ± 0.020 pmol/mg tissue for control, 1, and 3 mg/kg, respectively (n=4 mice per treatment). Limit of detection for cys-DA and cys-DOPAC were 0.0292 pmol and 0.0234 pmol, respectively, and are lower than what is reported in the literature. (B) Carbonyl formation was increased 57% and 90% in the striatum (STR) of mice dosed intraperitoneally with 1 or 3 mg/kg dieldrin, respectively. Data are presented as percentage of control values and represent mean + SEM (n=4 per treatment). (*p<0.05; overall p=0.0074). Cortex (CTX), Hippocampus (HIPPO), Midbrain (MB), Hypothalamus (HYPO), Cerebellum (CBL). (C) The redox potential (E_h) for glutathione was increased in the striatum of mice dosed with 3 mg/kg dieldrin (**p<0.01; overall p=0.0041). Mean values ± SEM for redox potentials were −238.2 ± 1.5, −233.4 ± 1.9, and −226.3 ± 2.1 mV for control, 1, and 3 mg/kg, respectively (n=4 mice per treatment).

(A) 1 and 3 mg/kg exposures resulted in a 12.4% and 14.7% decrease in ³H-WIN35,428 binding to DAT, indicating a decrease in DAT levels. Reductions in DAT levels and increased carbonyl formation are highly correlated (r²=0.978). Overall p=0.0017. Mean values ± SEM for binding were 841.0 ± 22.0, 737.0 ± 21.4, and 718.0 ± 17.3 fmol/mg protein for control, 1, and 3 mg/kg, respectively. (B) There was a 9.1% and 21.2% decrease in DAT-mediated ³H-dopamine uptake following 1 and 3 mg/kg exposure, indicating decreased DAT function. There is a strong correlation between reductions in dopamine uptake and increase carbonyl formation (r²=0.964) Overall p=0.0296. Mean values ± SEM for uptake were 251.2 ± 8.0, 228.5 ± 1.4, and 198.0 ± 8.1 pmol/mg/min for control, 1, and 3 mg/kg, respectively. (C) Dose-dependent decrease in striatal DAT protein expression as measured by western immunoblotting (16.4%, and 26.9% for 1 and 3 mg/kg, respectively; overall p=0.0389) Data are presented as percentage of control values and represent mean ± SEM (n=3–4 per treatment). (For all graphs, *p<0.05, **p<0.01). Representative western blots of DAT (D; 75 kDa) and a-tubulin (E; 55 kDa) to ensure equal protein loading.

(A) Striatal α-synuclein expression increased by 29.8 and 24.7% following 1 or 3 mg/kg exposure, respectively, as measured by western immunoblotting. (***p<0.001; overall p < 0.0001). Data are presented as percentage of control values and represent mean ± SEM (n=3–4 per treatment). Representative western blots of α-synuclein (B; 19 kDa) and a-tubulin (C; 55 kDa) to ensure equal protein loading.

(A) There is no significant neuronal loss in the SNc. Data expressed as mean ± SEM (n=4). (B) There is no significant change in TH levels as measured by western immunoblotting. Data are presented as percentage of control values and represent mean ± SEM (n=3–4 per treatment). Representative western blots of TH (C; 62 kDa ) and a-tubulin (D; 55 kDa) to ensure equal protein loading.