Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...

CONCLUSIONS
5) Intraperitoneal aluminium chloride exposure to rats for one week causes a
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significant and greater aluminium accumulation in cerebellum, cortex,
hippocampus and striatum, whereas a decrease in aluminium concentration is
reported in ventral midbrain.
6) Aluminium administered i.p. predominantly accumulates in the hippocampus,
whereas aluminium administered orally principally accumulates in the ventral
midbrain.
7) Aluminium accumulation in the brain and its distribution in the different areas of
the brain varie with the administration route used.
Chapter 3
8) Aluminium i.p. exposure to rats can create a situation of oxidative stress in most of
the brain areas studied.
9) Aluminium causes a significant increase in the levels of TBARS in ventral
midbrain, cortex and striatum, but particularly so in the cerebellum, while no
significant changes is noted in the hippocampus.
10) Aluminium provokes a significant increase in both PCC and PTC in the cerebellum,
ventral midbrain, and striatum, whereas a decrease is reported in the cortex and
hippocampus. The molecular mechanism involved in the lack of a direct correlation
between the increase observed in the PCC, and the “apparently” contradictory
increase in PTC has not been found out.
11) All the brain regional areas examined show similar behaviour patterns as
aluminium leads to a decrease of the enzyme activity of SOD, GPx, and CAT,
except in hippocampus where antioxidant enzymes activities increase.
12) Aluminium does not significantly alter the enzyme activities of either of SOD,
GPx, and CAT in vitro.