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has long been recognized as a major risk factor for ED in man. The prevalence
of ED in diabetic men are four times more than age-matched nondiabetic men, and
this difference increases with age (Maiorino et al., 2014). Experimental
and clinical studies have demonstrated that, the pathophysiology of diabetic ED
is multifactorial, consisting predominantly of vascular and neurological
insults as a result of hyperglycemia induced-metabolic imbalances (Brownlee,
2001). Autonomic
neuropathy can account for a decreased function of erectogenic nerves or an
altered balance of the pro-erectile and anti-erectile transmitters reaching the
cavernosal smooth muscle. The vascular supply of the penis is highly sensitive
to atherosclerotic changes, which are accelerated in diabetic individuals. Furthermore, in diabetic condition increases the level of arginase enzyme,
which inhibits the availability of L-arginine as substrate to decrease the
synthesis of nitric oxide (NO). In addition, denovo synthesis of diacyglycerol
promotes to protein kinase C activation, which further activates reaction
oxygen species (ROS). The effects of diabetes on the rat ejaculatory process,
which can lead to a decreased fertility rate in vivo (Scarano et
al., 2006), can be explained by a secondary complication of diabetes, an
autonomic neuropathy syndrome (Vinik et al., 2003).

hyperglycemic conditions have been reported to promote the generation of ROS
and nitrogen species (RNS), and to induce the formation of advanced glycation
end-products (AGE). Consecutively, this may cause changes in the
bioavailability of neuronal- and endothelial-derived NO, which may impair
vasorelaxation mechanisms in the diabetic corpus cavernosum (Agarwal et al.,
2006). Furthermore, a toxic molecule called malondialdehyde (MDA) produced by
ROS and causes by lipid peroxidation in cellular membrane. Whereas the MDA
level could represents the degree of lipid peroxidation and oxidative stress in
vivo.  Superoxide dismutase (SOD) is
another important enzyme that removes the superoxide radicals from the human
body. Excess amounts of ROS inactivate SOD and lead to decreased removal of
superoxide, which further increases the formation of peroxynitrite and reduces
the available NO concentration (Hirata et al., 2009). Hyperglycemia
is kwon to induce in?ammatory cytokines such as TNF-?, IL-1, and IL-6 (Arya et al., 2012) which may
contribute to diabetes induced testicular damage. It
has been demonstrated that under diabetic status, oxidative stress is a major
cause for loss of male germ cells since diabetic induction of testicular
apoptotic cell death was forbidden by either antioxidant treatment with
N-acetyl-L-cysteine or low-level ionizing radiation that induces up-regulation
of testicular antioxidants (Zhao et al., 2010).

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Naringenin, (5,7,4′-trihydroxyflavanone, Figure 1) belongs to the
class of flavonoids called the flavanones. The flavanones are abundant in
citrus fruits such as grapefruits and oranges. The role of NG and the related
citrus flavanone hesperetin in the treatment of disease has received
considerable attention, with particular interest as anticancer and
antiatherogenic compounds (Wilcox et al., 1999). NG is associated with
beneficial effects in osteoporosis, cancer and cardiovascular diseases
(Galluzzo et al., 2008). 

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