Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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Chapter | 23 Vitamins
Infection
EH
E
E
EH
ROO•
•OH
OH
•OOH
Giu
ROOH
GSH
NADP
Glu-6P
O 2
O 2
GSSG
NADPH
6p-Gluc
ROH
Drugs
RH
Superoxide
H 2 O 2
H 2 O 2 Dismutase
H 2 O
Glutathione reductase
b-Oxidation
Glutathione peroxidase
Catalase
Glucose 6-phosphate dehydrogenase
H 2 O
HMP
Cytosol
Lactate
CELL MEMBRANE
FIGURE 23-11 Vitamin E and antioxidant defense. A number of factors can influence the need for tocopherols in cells and subsequently their utilization
at a cellular level. Vitamin E acts as the last line of defense for lipid oxidation, primarily residing in lipid membranes. Enzymes such as superoxide
dismutases (catalyzes superoxide radicals to hydrogen peroxide), catalase (catalyzes hydrogen peroxide to water and oxygen), glutathione peroxidase
(catalyzes lipid and hydrogen peroxides to water or hydroxy-fatty acids), and related systems for oxidant defense (generation of reductants, such as
NADPH and reduced glutathione) also aid in providing additional oxidant defense. Without intracellular control of reactive oxygen species, such as
hydrogen peroxide or hydroxide radicals, polyunsaturated lipids are targets for oxidation.
Vitamin E enters cells by processes similar to those
for LDL uptake (Aguie, 1995; Traber et al., 1993, 1994a,
1994b, 1994c ). LDL membrane receptors, through receptor-mediated
endocytosis, appear responsible for vitamin E
uptake by scavenger receptor B type I and LDL receptors.
Efflux from cells is less well understood but appears to be
dependent on transporters in the ABCA1 transporter family
(ATP-requiring transporters associated with cholesterol
transport). Once in cells, vitamin E is incorporated into
liquid membranes. About 40% of vitamin E is found in
nuclear membranes; the remaining 60% is divided between
lysosomal, mitochondrial and the outer cell wall membranes
( Traber, 2007 ).
3 . Requirements and Functions
The nutritional status of vitamin E is often difficult to
assess. A number of factors can influence the concentration
of tocopherols in cells. As noted, vitamin E acts as
the last line of defense for lipid oxidation, primarily residing
in lipid membranes. Consequently, enzymes such as
superoxide dismutases, catalase, glutathione peroxidase,
and related systems for oxidant defense can moderate the
absolute need for vitamin E ( Fig. 23-11 ). Further high
dietary intakes of polyunsaturated dietary fats may increase
the vitamin E requirement, because of their eventual deposition
in cell membranes. Naturally occurring deficiencies
of vitamin E occur in cats given human-grade canned
tuna (which is not fortified with vitamin E). Deficiencies
can also occur in cats given fish-based diets unless they
are highly fortified with vitamin E. Proper handling of fish
is essential to prevent the PUFA s in fish oil from readily
oxidizing following their harvesting and processing. The
requirement of most animals is on the order of 25 to 50 mg
per kilogram dry diet or 4 to 8 mg per 1000 kcal or 4.2 MJ.
At the cellular level, vitamin E deficiency promotes
increased lipid peroxidation, making cells more vulnerable
to oxidative injury. Fortunately clinical manifestations
of chronic vitamin E deficiency are rare and are usually
seen only when fat malabsorption is present. In these cases,
the neuromuscular, vascular, and reproductive systems
may be affected. Vitamin E deficiency signs include