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Introduction
Thyroid hormones (TH) are required for the normal function of most tissues of
the body, playing essential roles in growth, development, differentiation, and
metabolism, with major effects on O 2 consumption and metabolic rate (Videla,
2000). Hyperthyroidism is associated with an increased metabolic rate due to
increments in the rate of oxygen consumption in target tissues. Acceleration of
aerobic metabolism by thyroid hormones enhances the generation of oxidative
stress (Aydin, 2006) Oxidative stress is regarded as a pathogenic factor in
hyperthyroidism. Clinical and experimental studies reported increased levels of
free oxygen radicals and a decreased antioxidant status in thyrotoxicosis
(Karbownik, and Lewinski, 2003).
Free oxygen radicals are general mediators of signal transduction pathways, which
are able to induce cytokine production from various cell types (Siddiqi et al
.,1999). Studies attesting to the role of antioxidants, of which potentially inhibit the
activation of oxidant-mediated transcription factors, reported that these
antioxidants also prevent the transcriptional activation of inflammatory cytokines
(PaoloDeVito et al., 2011).
Oxidative stress accompanying hyperthyroidism is caused by increased synthesis
of reactive oxygen species (ROS) and changes in the antioxidant defense system
(Lampka et al., 2006). ROS have a high reactivity potential, therefore they are
toxic and can lead to oxidative damage in cellular macromolecules such as
proteins, lipids and DNA (Araujo et al .,2006) .In fact, the cell contains a variety
of substances capable of scavenging the free radicals, protecting them from
harmful effects. Among the enzymatic antioxidants, are glutathione reductase
(GR), glutathione peroxidase (GPx), catalase (CAT),superoxide dismutase (SOD),
while the non-enzymatic antioxidants are glutathione(GSH), vitamin E, vitamin C,
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β-carotene, and flavonoids (Messarah et al., 2007). When ROS generation exceeds
the antioxidant capacity of cells, oxidative stress develops (Sies, 1997). This
phenomenon has been related to many pathological conditions (Freeman and
Crapo, 1982; Halliwell and Gutteridge, 1990) and it has also been suggested that
some complications of hyperthyroidism are due to thyroid hormone-induced
oxidative stress in target tissues (Asayama, and Kato, 1990).
Life means a continuous struggle for energy, which is required to fight against
entropy. The most effective way to obtain energy is oxidation. Oxidative processes
predominantly occur in mitochondria (Mircescu, 2008). On the other hand,
mitochondria are one of the favorite targets of thyroid hormones. During thyroid
hormone synthesis, there is a constant production of hydrogen peroxide, which is
absolutely indispensable for iodine oxidation in the presence of thyroid peroxidase.
In recent years, the possible correlation between impaired thyroid gland function
and reactive oxygen species has been increasingly taken into consideration (Vitale
et al., 2000). Thyroid hormones are the most important factors involved in the
regulation of the basal metabolic state, as well as in the oxidative metabolism
(Asayama, and Kato, 1990).
Thyroid hormones can cause many changes in the number and activity of
mitochondrial respiratory chain enzymes, which may result in the increased
generation of ROS (Mano et al., 1995; Guerrero et al .,1999). Experimental studies
and epidemiological data suggest that hyperthyroidism is associated with a general
increase in tissue oxidative stress. Great controversy exists as to whether
hyperthyroidism is associated with an increase or a decrease in the activities of
antioxidant enzymes (Seven et al ., 1996 ; Komosinska-Vassev et al., 2000).
Vitamin E is a potent lipid soluble antioxidant in biological systems with the
ability to directly quench free radicals and function as membrane stabilizer
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(Subudhi et al., 2008). Antioxidants treatments might be helpful in reducing the
oxidative damage due to hyperthyroidism.
The antioxidant protection of natural plants is a promising therapeutic remedy
for free radical pathologies (Halverson et al .,2002 ). Among myriad natural plants,
red cabbage (RC) (Brassica oleracea var capitata) and other Brassica vegetables,
vegetables endemic to the Mediterranean region, have been found to have
antioxidant, antihyperglycemic( Roman-Ramos et al .,1995 ; Grover et al .,2003 ;
Yokozawa et al .,2003 ), anticancer (Fahey et al .,1997; . Komatsu et al .,2002 ;
Fowke et al .,2003),and hypocholesterolemic (Komatsu et al .,1998) properties.
RC extract has also preventive oxidative stress induced in livers and brains of
animals exposed to paraquate (Igarashi et al., 2000 ) N-methyl-D-aspartate (Lee et
al., 2002).
The principle constituents of RC are isothiocyanates (glucosinolate), vitamins
A, B, C and anthocyanins. (Repetto and Leusy,2002 ; Jagdish et al., 2006 ).
Anthocyanins, a group of phenolic natural pigments present in RC, were found to
have the strongest antioxidizing power of 150 flavonoids (Barbara et al., 2008).
Looking into overall literature, the objective of the present investigation is to
evaluate the possible relationship between the dynamics of oxidative stress and
thyroid hormones levels under inflammatory cytokine induction as well as to verify
if thyroxine has a role in the induction of oxidative stress. Aim of this study to
investigate effect of the RCE on the thyroid hormone, cytokine level, lipid profile
level, liver enzyme level, enzymatic antioxidant level and histological change in
thyroid gland.
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