Volume 23 • Issue 01 • 2019
with a variety of antioxidants that serve to
counterbalance the effect of oxidative stress.
Antioxidants can be divided into enzymatic and
non-enzymatic antioxidants. events.
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Enzymatic antioxidants
The key enzymatic antioxidants of this defence
system by which free radicals are removed
include:
Superoxidase dismutase (SOD),
Glutathione peroxidase (GPX)
Catalase.
Superoxide dismutase (SOD) is an enzyme
with a generalised presence in the body and is
influenced by Cu, Zn and Mn.
Glutathione peroxidase (GSH-Px) is believed to
be the most important extracellular antioxidant
enzyme in mammals and is Se dependent.
Catalase is an antioxidant enzyme present in
cytoplasm that acts as a catalyst for the conversion
of hydrogen peroxide to oxygen and water.
Non-enzymatic antioxidants.
Non-enzymatic antioxidants are known as
synthetic antioxidants or dietary supplements
and are low-molecular weight compounds which
include the following.
Vitamin C (Ascorbic acid). A water soluble vitamin
that provides intracellular and extracellular
antioxidant protection.
Vitamin E (α-Tocopherol). A lipid soluble vitamin
and is in principal a membrane bound antioxidant
in cells.
β- Carotene. These are pigments found in plants
and react with superoxide.
Uric acid. An important antioxidant in bovine
erythrocytes (red blood cells) and act as a free
radical scavenger.
Glutathione (GSH). Abundant in all cell
compartments and is important for protection of
cell membrane.
Reactive oxygen species in the male
reproductive system.
Cellular generation of reactive oxygen species
(ROS) has now been demonstrated in spermatozoa
of various mammalian species, including the rat,
mouse, rabbit, horse, bull and humans and can be
either beneficial or detrimental to reproductive
Reactive oxygen species are generated by sperm
metabolism and are required for maturation,
capacitation and acrosome reaction but they also
modify cellular compounds.
The mechanisms by which oxidative stress
limits the functional competence of mammalian
spermatozoa involve:
The peroxidation of lipids,
The induction of oxidative DNA damage,
The formation of protein adducts.
ROS production in these cells involves electron
leakage from spermatozoa mitochondria and
consequently spermatozoa lose their motility,
DNA integrity and vitality. This pathway also
influences the female tract’s immune response to
sperm antigens and future fertility.
Currently oxidative stress is believed to be an
important cause of idiopathic male infertility
since gametes are susceptible to OS. Defective
sperm function is the most prevalent cause of
male infertility and statistics from the United
States indicate that up to 40% of infertile men
have elevated levels of ROS in their seminal
plasma.
Spermatozoa are equipped with antioxidant
defence mechanisms and are likely to quench
ROS, thereby protecting gonadal cells and
mature spermatozoa from oxidative damage.
When uncontrolled production of ROS exceeds
the antioxidant capacity of the seminal plasma
it results in oxidative stress. Spermatozoa
are unable to restore the damage induced by
oxidative stress because they lack the necessary
cytoplasmic-enzyme repair systems which
makes spermatozoa unique in their susceptibility
to ROS.
This is due to the fact that their cell membranes
are rich in polyunsaturated fatty acids (PUFA),
rendering them highly susceptible to oxygen
induced damage mediated by lipid peroxidation
(LPO).This process causes axonal damage,
decreased sperm viability and increased mid-
piece sperm morphological defects, all of which
contribute to decreased sperm motility.
The effect of trace mineral supplementation on
semen quality of bulls needs further investigation.
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