Morsy, G. M., K. A. E. Ela, and A. A. Elmoneam, "Studies on fate and toxicity of nanoalumina in male albino rats: 2. Oxidative stress in the brain, liver and kidney", Toxicologyand Industrial Health, pp. 1-24, 2013. Abstractoxidative_stress.pdf

The present work aimed to evaluate the oxidative st
ress of nanoalumina
(aluminium oxide nanoparticles, Al2O3-NPs) with a d
iameter <13nm
(9.83±1.61 nm) as assessed by the perturbations in
the enzymatic and
non-enzymatic antioxidant as well as lipid peroxida
tion (LPO) in the brain,
liver and kidney of male albino rats, after two day
s of injection of a single-
acute dose (3.9g or 6.4g or 8.5g Al2O3/kg), and a s
ub-lethal dose of 1.3g
Al2O3/kg/2day, over a periods of 28 days. According
to two-ways ANOVA,
superoxide dismutase (SOD), catalase (CAT) and glut
athione peroxidase
(GPx) activities as well as the levels of glutathio
ne (GSH) and LPO were
significantly affected by the injected-doses, organ
s and their interactions.
On the other hand, in sub-lethal experiments, these
parameters were
affected by the experimental periods, organs and th
eir interactions.
Regression analysis confirmed that the activities o
f SOD, CAT, GPx and
GSH levels in the brain, liver and kidney were inve
rsely proportional with
the acute doses, the experimental periods, and alum
inium accumulated in
these tissues, whereas levels of LPO exhibited a po
sitive relationship.
Correlation coefficient indicated that oxidative st
ress mainly depends on
aluminium accumulated in the studied organs, follow
ed by injected doses
and the experimental periods. In comparison with th
e corresponding
controls, the acute and sub-lethal doses of Al2O3-N
Ps caused significant
inhibition of the brain, hepatic and renal SOD, CAT
, GPx activities and a
severe marked reduction in the concentrations of GS
H that were associated
with a significant elevation in the levels of malon
dialdehyde MDA (LPO). In
conclusion, our data indicated that rats-injected w
ith nanoalumina suffered
from the oxidative stresses that were dose and time
dependent. In
addition, Al2O3-NPs released into the biospheres co
uld be potentiating a
risk to the environment and causing hazard effects
on living organisms,
including mammals.

Morsy, G. M., S. M. Rawy, and M. M. Elshibani, "Lethality, accumulation and toxicokinetics of aluminum in some tissues of male albino rats", Toxicology and Industrial Health, vol. 29(3): 254-263 (first published on February 8, 2012) , issue On line Issue April 2013, pp. 254-263, 2013. Abstractlethality_accumulation_and_toxicokinetics_of_aluminum_in_some_tissues_of_male_albino_rats.pdf

In the present work, the lethality percentiles including median lethal doses (LD50), accumulation, distribution and toxicokinetics of aluminum in the liver, kidney, intestine, brain and serum of male albino rats, following a single oral administration were studied throughout 1, 3, 7, 14 and 28 days. The estimated LD50 at 24 h was 3.45 g Al/kg body weight (b.wt.). The utilized dose of Al was 1/50 LD50 (0.07 g Al/kg b.wt.). Aluminum residues, in Al-treated rats, were significantly decreased in response to the experimental periods and were negatively correlated with time. In addition, the hepatic, renal, intestinal, brain and serum Al contents were significantly higher than the corresponding controls at all experimental periods, except the brain that showed significant depletion when compared with its corresponding control after 28 days. Kinetically, the highest average of Al area under concentration - time curves (AUCtotal, μg/g day) and area under moment concentration - time curves (AUMCtotal, µg/g day(2)) recorded in the brain followed by kidney, serum, intestine and liver. The longest elimination half-life time (t 1/2, day) and the mean residence time (MRT, day) were recorded in the brain followed by the liver, kidney, serum and intestine. On the other hand, the slowest clearance rates (Cls, L/day) of Al, in order, were recorded in brain, kidney, serum, intestine and the liver. The elimination rate constant (Lz, day(-) (1)) of Al from the brain was less than that in the intestine and serum was less than that in the liver and kidney. The computed maximum concentrations (C max) of Al in the intestine > kidney > serum > brain > liver were recorded after 3, 3.8, 2.2, 5.4 and 3.8 days, respectively. The computed starting concentration (C 0, μg) of Al in serum was higher than its level in the intestine followed by the brain, kidney and liver.

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