الفهرس 
Physical and chemical properties of polychlorinated dibenzo-pdioxinsOnly 14 pages are availabe for public view
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Abstract
Environmental pollution is reaching worrying proportions worldwide, as
urbanization and industrialization along with economic development
increased energy consumption and waste discharges.
Polychlorinated dibenzo-p-dioxins (PCDDs) are among the most dangerous
wastes discharged and received an increasing attention as environmental
pollutants as they belong to persistent organic pollutants (POPs) which are
resistant to chemical and biological degradation and biomagnified through
food chain.
The most critical congener is 2, 3, 7, 8 tetrachlorodibenzo-p-dioxin
(TCDD) among all polychlorinated dibenzo-p-dioxins (PCDDs).
TCDD is an unintended by product of many industries like chlorine paper
bleaching, steel industry and chemical manufacture of chlorinated
compounds but the main source of dioxin is open incineration of chlorine
containing organic wastes.
The most consistent toxic effects of dioxin-type are hyperlipidemia, body
weight loss (particularly body fat loss called wasting syndrome in animals),
hepatotoxicity (abnormal liver functioning due to liver injury), changes in
carbohydrate metabolism (diabetes), and lipid peroxidation (increased
formation of reactive oxygen species).
Reducing dietary exposure to dioxins among the most vulnerable segments of
the population (i.e., pregnant women and infants) is an effective strategy for
reducing body burdens in future generations as few methods have been
explored for the remediation of animals exposed to dioxins using nutritional
treatments.
Chitosan is a naturally occurring cationic biopolymer comprised of
glucosamine, and can be produced by the deacetylation of chitin which is the
second most abundant polysaccharide after cellulose in the world It has many great effects as an antioxidative, hepatoprotective, detoxifying,
anti-inflammation and hypolipidemic agent.
The aim of this study was to explore the importance of chitosan feeding
as a food additive and it’s the effectiveness of 3 multiplied doses of chitosan
(as1.2, 2.4 and 3.6 g chitosan/ kg diet) in alleviating the oxidative,
hyperlipidemic, hepatotoxic and liver histopathological effects caused by
single oral dose of 5μg TCDD/ kg B. wt. in adult male Sprague Dawley (SD)
weighed 120-140 gm
Experimental animals were divided into eight groups
Group 1 (G1): fed standard control diet (negative control).
Group2 (G2): fed standard diet and gavaged with single oral dose of
TCDD (5 μg/kg B. wt.) at the beginning of the experiment (dioxin
positive control).
Group 3, 4 and 5 (G3, G4 and G5): fed standard diet supplemented
with either 1.2, 2.4 or 3.6 g chitosan / kg diet (Chitosan 1 or 2 or 3).
Group 6, 7and 8 (G6, G7 and G8): fed standard diet supplemented
with either 1.2, 2.4 or 3.6 g chitosan / kg diet and given single oral
dose of TCDD (5 μg/kg B. wt.) (Chitosan 1 or 2 or 3+ TCDD).
Diets and water were administered adlibitium to rats for six weeks. Animals
and diets were weighed twice weekly to determine body weight change (g/
feeding period), total feed intake (g/ feeding period) were recorded to
calculate feed efficiency ratio.
After 6 weeks, rats were sacrificed after ether anesthesia. Blood samples
were collected in either EDTA coated tubes to determine hematological
indices as (Hb, HCT, MCH, MCV, RBCs, WBCs and platelets) or in
uncoated tubes to determine blood GSH and RBCs-SOD. The remaining
blood was collected in heparin free tubes to separate serum for determination
of liver functions (ALT, AST and Alk-P), lipid profile (cholesterol,
triacylglycerols, HDL-C and LDL-C) and protein profile (total roteinprotein, albumin, globulin and A/G ratio). Relative weight of livers was assigned,
then three parts were kept frozen for determination of liver GSH, MDA and
vitamin A. Another part of liver was prepared for histological examination.
Effect of chitosan on total feed intake, body weight change and feed
efficiency ratio:
The highly significant decrease in feed intake in rats gavaged once with
dioxin in G2 may be due to anorexia and less appetite caused by dioxin.
The continuing decrease _but not significant_ in feed intake when chitosan
was fed to rats gavaged with dioxin G6, G7 and G8 due to that chitosan is
considered a dietary fiber so make bulk in stomach that decreases feed intake.
Oral dioxin caused a highly significant decrease in body weight in G2 and
this is attributed to that dioxin induces a diabetic like syndrome causing
wasting of stored body fats. Chitosan alone in G3, G4 and G5 or in rats
gavaged with single oral dose of dioxin in G6, G7 and G8 caused a
significant decrease in body weight because it is a leanless agent (it decrease
leptin hormone responsible for the extent of obesity by regulating energy
expenditure and food intake through the central nervous system) and increase
fecal excretion of fats.
Feed efficiency ratio decreased significantly in different groups due to
disturbance occurred in food intake and body weight changes.
Effect of chitosan on relative weight of liver:
The highly significant increase in relative liver weight following dioxin
oral dose in G2 is due to increase in fatty liver vocalization. The decrease
caused in G6, G7 and G8 is due to lipolysis caused by chitosan.
Effect of chitosan on antioxidant status and oxidative stress in blood and
liver:
Blood and liver GSH significant decrease in rats gavaged once with
dioxin G2 is due to that dioxin induced production of free radicals disables
antioxidant enzyme activities.albumin, globulin and A/G ratio). Relative weight of livers was assigned,
then three parts were kept frozen for determination of liver GSH, MDA and
vitamin A. Another part of liver was prepared for histological examination.
Effect of chitosan on total feed intake, body weight change and feed
efficiency ratio:
The highly significant decrease in feed intake in rats gavaged once with
dioxin in G2 may be due to anorexia and less appetite caused by dioxin.
The continuing decrease _but not significant_ in feed intake when chitosan
was fed to rats gavaged with dioxin G6, G7 and G8 due to that chitosan is
considered a dietary fiber so make bulk in stomach that decreases feed intake.
Oral dioxin caused a highly significant decrease in body weight in G2 and
this is attributed to that dioxin induces a diabetic like syndrome causing
wasting of stored body fats. Chitosan alone in G3, G4 and G5 or in rats
gavaged with single oral dose of dioxin in G6, G7 and G8 caused a
significant decrease in body weight because it is a leanless agent (it decrease
leptin hormone responsible for the extent of obesity by regulating energy
expenditure and food intake through the central nervous system) and increase
fecal excretion of fats.
Feed efficiency ratio decreased significantly in different groups due to
disturbance occurred in food intake and body weight changes.
Effect of chitosan on relative weight of liver:
The highly significant increase in relative liver weight following dioxin
oral dose in G2 is due to increase in fatty liver vocalization. The decrease
caused in G6, G7 and G8 is due to lipolysis caused by chitosan.
Effect of chitosan on antioxidant status and oxidative stress in blood and
liver:
Blood and liver GSH significant decrease in rats gavaged once with
dioxin G2 is due to that dioxin induced production of free radicals disables
antioxidant enzyme activities.