Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...
Mechanisms of aluminium neurotoxicity in oxidative stress-induced ... Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...
CHAPTER 3 Effects of aluminium administration on brain lipid peroxidation and protein oxidation in 6-OHDA-lesioned rats and controls 130 Once again, the concentration of TBARS was used as an index of lipid peroxidation in striatum and ventral midbrain (Fig. 5A). Both regions of animals i.p. injected with aluminium alone (subgroup D) showed a statistical difference in TBARS production compared to non-lesioned (subgroup C) control rats (+40% in ventral midbrain and +16% in striatum). Intraventricular injection of 6-OHDA resulted in a significant increase in TBARS concentration in both striatum and ventral midbrain when compared to control rats (+29% and +76%, respectively) and to animals treated with aluminium (+12% and +26%, respectively)). Ventral midbrain and striatum TBARS levels in rats i.p. treated with aluminium and intraventricularly injected with 6- OHDA were +107% and +40% (respectively) increased in respect to control animals. When compared to rats only treated with aluminium (i.e. without 6-OHDA; subgroup D), the TBARS levels of subgroup-F rats were markedly increased in both regions (+47% in ventral midbrain and +21% in striatum) and there were also significant differences when compared with subgroup E, rats only lesioned with 6-OHDA (+17% in ventral midbrain and +8% in striatum). Protein oxidation was assessed by the determination of PCC and PTC in the samples of striatum and ventral midbrain. No significant changes were noticed in the PTC (Fig. 5C) except for rats lesioned with 6- OHDA when compared with animals treated only with aluminium (–11%). By contrast, as shown in Fig. 5B, intraventricular injection of 6-OHDA induced a significant increase in the PCC in striatum and ventral midbrain (+33% and +22%, respectively) as compared with control rats. Treatment with aluminium (subgroups D) revealed a significant difference in ventral midbrain and striatum as compared to control rats (+11% and +18%, respectively). On the other hand, in subgroup F (animals treated with aluminium and lesioned with 6-OHDA) the PCC was reduced in both regions (–16% in ventral midbrain and striatum) as compared to the rats lesioned with 6-OHDA.
CHAPTER 3 In vitro effects of aluminium on the lipid peroxidation and protein oxidation induced by 6-OHDA autoxidation in brain mitochondrial preparations As depicted in Fig. 6A, the incubation of 6-OHDA (10 �M) with brain mitochondria at 37°C for 20 min induced a significant production of TBARS when compared to the mitochondria (Mit) and Mit+Al controls (+91% and +116%, respectively). Significant changes in TBARS production (+100%, +127%) were observed when the autoxidation of 6-OHDA occurred in the presence of Al 3+ (5 �M) as compared to the Mit and Mit+Al controls, respectively. However, the presence of aluminium did not significantly affect the level of TBARS found after the incubation of 6-OHDA in mitochondrial preparations when compared to the Mit+6-OHDA control. The incubation of 6-OHDA (10 �M) with brain mitochondria at 37°C for 20 min induced a significant increase in the PCC (+7%; Fig. 6B) as compared to the Mit control. However, the results obtained in the presence of Al 3+ (5 �M) were not significantly different from control values. As can be seen in Fig. 6C, the PTC exhibited a significant reduction (–9%) in the incubation of 6-OHDA (10 �M) with brain mitochondria at 37°C for 20 min when compared with that obtained in the control with mitochondria alone and Mit+Al 3 . The presence of aluminium had no significant effect on the PTC found with mitochondrial incubations when compared to controls. In vitro effects of aluminium on the enzyme activities of GPx, SOD, CAT, and MAO The results regarding the effect of aluminium on the in vitro activities of GPx, CAT, SOD, MAO-A and MAO-B enzymes are displayed in Table 1. In all cases, no significant differences were detected between assays performed in the presence and in the absence of Al 3+ (10, 50, 100 �M) 131
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CHAPTER 3<br />
Effects <strong>of</strong> <strong>alum<strong>in</strong>ium</strong> adm<strong>in</strong>istration on bra<strong>in</strong> lipid peroxidation and<br />
prote<strong>in</strong> oxidation <strong>in</strong> 6-OHDA-lesioned rats and controls<br />
130<br />
Once aga<strong>in</strong>, the concentration <strong>of</strong> TBARS was used as an <strong>in</strong>dex <strong>of</strong> lipid<br />
peroxidation <strong>in</strong> striatum and ventral midbra<strong>in</strong> (Fig. 5A). Both regions <strong>of</strong> animals i.p.<br />
<strong>in</strong>jected with <strong>alum<strong>in</strong>ium</strong> alone (subgroup D) showed a statistical difference <strong>in</strong> TBARS<br />
production compared to non-lesioned (subgroup C) control rats (+40% <strong>in</strong> ventral<br />
midbra<strong>in</strong> and +16% <strong>in</strong> striatum). Intraventricular <strong>in</strong>jection <strong>of</strong> 6-OHDA resulted <strong>in</strong> a<br />
significant <strong>in</strong>crease <strong>in</strong> TBARS concentration <strong>in</strong> both striatum and ventral midbra<strong>in</strong><br />
when compared to control rats (+29% and +76%, respectively) and to animals treated<br />
with <strong>alum<strong>in</strong>ium</strong> (+12% and +26%, respectively)). Ventral midbra<strong>in</strong> and striatum<br />
TBARS levels <strong>in</strong> rats i.p. treated with <strong>alum<strong>in</strong>ium</strong> and <strong>in</strong>traventricularly <strong>in</strong>jected with 6-<br />
OHDA were +107% and +40% (respectively) <strong>in</strong>creased <strong>in</strong> respect to control animals.<br />
When compared to rats only treated with <strong>alum<strong>in</strong>ium</strong> (i.e. without 6-OHDA; subgroup<br />
D), the TBARS levels <strong>of</strong> subgroup-F rats were markedly <strong>in</strong>creased <strong>in</strong> both regions<br />
(+47% <strong>in</strong> ventral midbra<strong>in</strong> and +21% <strong>in</strong> striatum) and there were also significant<br />
differences when compared with subgroup E, rats only lesioned with 6-OHDA (+17%<br />
<strong>in</strong> ventral midbra<strong>in</strong> and +8% <strong>in</strong> striatum). Prote<strong>in</strong> oxidation was assessed by the<br />
determ<strong>in</strong>ation <strong>of</strong> PCC and PTC <strong>in</strong> the samples <strong>of</strong> striatum and ventral midbra<strong>in</strong>. No<br />
significant changes were noticed <strong>in</strong> the PTC (Fig. 5C) except for rats lesioned with 6-<br />
OHDA when compared with animals treated only with <strong>alum<strong>in</strong>ium</strong> (–11%). By contrast,<br />
as shown <strong>in</strong> Fig. 5B, <strong>in</strong>traventricular <strong>in</strong>jection <strong>of</strong> 6-OHDA <strong>in</strong>duced a significant<br />
<strong>in</strong>crease <strong>in</strong> the PCC <strong>in</strong> striatum and ventral midbra<strong>in</strong> (+33% and +22%, respectively) as<br />
compared with control rats. Treatment with <strong>alum<strong>in</strong>ium</strong> (subgroups D) revealed a<br />
significant difference <strong>in</strong> ventral midbra<strong>in</strong> and striatum as compared to control rats<br />
(+11% and +18%, respectively). On the other hand, <strong>in</strong> subgroup F (animals treated with<br />
<strong>alum<strong>in</strong>ium</strong> and lesioned with 6-OHDA) the PCC was reduced <strong>in</strong> both regions (–16% <strong>in</strong><br />
ventral midbra<strong>in</strong> and striatum) as compared to the rats lesioned with 6-OHDA.
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