X-Message-Number: 24665
Date: Sun, 19 Sep 2004 13:24:52 -0700 (PDT)
From: Doug Skrecky <>
Subject: should naringin be taken before cryopreservation?

J Inorg Biochem. 2004 Aug;98(8):1457-64
The kinetics and mechanisms of reactions of iron(III) with caffeic acid,
chlorogenic acid, sinapic acid, ferulic acid and naringin.
 The kinetics and mechanisms of the reactions of iron(III) with the
hydroxy cinnamic acid based ligands caffeic, chlorogenic, sinapic and
ferulic acids and the flavonoid naringin have been investigated in
aqueous solution. The mechanisms for caffeic and chlorogenic acid are
generally consistent with the formation of a 1:1 complex that subsequently
decays through an electron transfer reaction. On reaction with iron(III),
ferulic and sinapic acids undergo an electron transfer without the prior
formation of any complex. There was no evidence of electron transfer
occurring in the complex formed when iron(III) is reacted with naringin.
Rate constants for [Formula: see text] (formation) and [Formula: see
text] (dissociation) have been evaluated for the complex formation
reactions of [Fe(H(2)O)(6)(OH)]( 2+) with caffeic acid, chlorogenic acid
and naringin. Analysis of the kinetic data yielded stability constants,
equilibrium constants for protonation of the iron(III) chlorogenic acid
complex initially formed, together with the rate co nstants for complex
decomposition through intramolecular electron transfers and in the case
of caffeic acid and chlorogenic acid, rate constants for the
iron(III) assisted decomposition of the initial complex formed. Some of
the suggested mechanisms and calculated rate constants are validated

Pharmacol Res. 2004 Aug;50(2):187-93
The effect of naringin, a bioflavonoid on ischemia-reperfusion induced
renal injury in rats.
 There is increasing evidence to suggest that toxic oxygen radicals play a
role in the pathogenesis of ischemia/reperfusion (I/R) injury in the
kidney. This study was designed to investigate the effects of naringin
(Ng), a bioflavonoid in I/R induced renal failure in rats. The protective
effect of naringin against the damage inflicted by reactive oxygen species
(ROS) during renal I/R was investigated in Sprague-Dawley rats using
histopathological and biochemical parameters. In one set of experiments
animals were unilaterally nephrectomized, and subjected to 45 min of left
renal pedicle occlusion and in another set both the renal pedicles were
occluded for 45 min followed by 24h of reperfusion. Naringin (400 mg
kg(-1), p.o.) was administered 60 min prior to ischemia. At the end of
the reperfusion period, rats were sacrificed. Thiobarbituric acid
reactive substances (TBARS), reduced glutathione (GSH) levels, catalase
(CAT), and superoxide dismutase (SOD) activities were determined in renal
tissue. Serum creatinine and blood urea nitrogen (BUN) concentrations
were measured for the evaluation of renal function. Ischemic control
animals demonstrated severe deterioration of renal function, renal
morphology and a significant renal oxidative stress. Pretreatment of
animals with naringin markedly attenuated renal dysfunction,
morphological alterations, reduced elevated TBARS levels and restored the
depleted renal antioxidant enzymes. The findings imply that ROS play a
causal role in I/R induced renal injury and naringin exert renoprotective
effects probably by the radical scavenging and antioxidant activities.

J Cardiovasc Pharmacol. 2001 Dec;38(6):947-55.
Naringin has an antiatherogenic effect with the inhibition of
intercellular adhesion molecule-1 in hypercholesterolemic rabbits.
 Naringin, a bioflavonoid found in citrus fruit peel, is known to have an
antioxidative effect, but its effect on atherosclerosis has not been
studied. This study evaluated the effect of naringin on blood lipid
levels and aortic fatty streaks, and its action mechanism in
hypercholesterolemic rabbits. Male New Zealand white rabbits were fed a
0.25% cholesterol diet and divided into an untreated group (n = 4), a
naringin-treated group (n = 5; 500 mg/kg per day), and a
lovastatin-treated group (n = 5; 20 mg/kg per day). After 8 weeks, blood
was sampled and analyzed biochemically. Aorta and liver were harvested and
examined histologically. Cholesterol level in rabbits fed the 0.25%
cholesterol diet reached 17 times normal and decreased in the rabbits fed
naringin and lovastatin, whose effects were not statistically significant
(p > 0.05). However, both naringin and lovastatin effectively
decreased the area of fatty streak in thoracic aorta on macroscopic
analysis (p < 0.05) and significantly reduced subintimal foam cell
infiltration on microscopic morphometry (p < 0.05). These foam cells were
macrophages on immunohistochemical analysis. Naringin treatment inhibited
hypercholesterolemia-induced intercellular adhesion molecule-1 (ICAM-1)
expression on endothelial cells. Hypercholesterolemia caused fatty liver
and elevation of liver enzymes, which was prevented by naringin but not
by lovastatin. Naringin significantly reduced fatty streak formation and
neointimal macrophage infiltration and also inhibited the expression of
ICAM-1 in endothelial cells, suggesting that suppression of ICAM-1
contributed to the antiatherogenic effect. Naringin, unlike lovastatin,
has a hepatoprotective action.

Cell Death Differ. 2000 Aug;7(8):739-46.
Prevention of toxin-induced cytoskeletal disruption and apoptotic liver
cell death by the grapefruit flavonoid, naringin.
 The protein phosphatase-inhibitory algal toxins, okadaic acid and
microcystin-LR, induced overphosphorylation of keratin and disruption of
the keratin cytoskeleton in freshly isolated rat hepatocytes. In
hepatocyte cultures, the toxins elicited DNA fragmentation and apoptotic
cell death within 24 h. All these toxin effects could be prevented by the
grapefruit flavonoid, naringin. The cytoprotective effect of naringin was
apparently limited to normal hepatocytes, since the toxin-induced
apoptosis of hepatoma cells, rat or human, was not prevented by the
flavonoid.

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