AntidotesTreatmentDetoxification Green Tea Extract by benbenzhou


More Info

1. Singh J., Rai M., Upadhyay AK., Bahadur A., Chaurasia SNS., Singh KP (Indian
Institute of Vegetable Research, Varanasi-221 005, India): Antioxidant phytochemicals
in broccoli (Brassica oleracea L. Var italica Plenck) cultivars. J Fd Sci Technol,
43(4), 2006, 391-393. [20 Ref]

 Six different cultivars of broccoli were analyzed for the major antioxidant
phytochemicals. Significant differences (p<0.05) were observed amongst the cultivars for
vitamin C, B-carotene, lutein, a-tocopherol and phenolic contents at edible maturity
stage. Vitamin C content ranged from 25.5 to 82.3 mg/100 g; maximum was in NS-50
(82.3 mg/100g) and Lucky had minimum (25.5 mg/100g). TheB-carotene and lutein
contents ranged from 0.48 to 1.13 mg/100g and from 0.41-1.02mg/100g, respectively).
Vitamin E (a-tocopherol) contents ranged from 0.22 to 0.68mg/100 g; maximum
tocopherol was in 'Sultan' (0.68mg/100g). The phenolic content ranged from 44.5 to 82.9
mg/100g; maximum was in 'Sultan' (82.9 mg/100 g) and minimum in 'Hybrid No2'

2. Suntres ZE., Lui EMK (Medical Sciences Division, Northern Ontario School of
Medicine Lakehead University Oliver Read, Thunder Bay, Ont. Canada P7B 5El,
Canada):     Antioxidant effect of zinc and zinc-metallothionein in the acute
cytotoxicity of hydrogen peroxide in Ehrlich ascites tumour cells. Chem Biol Interact,
162(1), 2006, 11-13. [60 Ref]

 This study was concerned with the role of zinc (Zn) and zinc-MT) in oxidative stress.
Hydrogen peroxide induced oxidative injury was examined in Ehrlich ascites tumour
cells isolated from control host mice, mice pretreated with 10 mg/kg ZnSO4 (i.p.) to
increase cellular Zn/Zn-MT levels, and mice exposed to Zn-deficient diet to reduce the
cellular Zn/Zn-MT levels. The results of the present study showed that Ehrlich cells with
seven-fold differences in Zn-MT concentrations could be obtained by manipulating the
Zn status of host mice and that high Zn and Zn-MT levels can make Ehrlich cells more
resistant to H2O2-induced oxidative injury (cell viability, lipid peroxidation, [Ca2+]i)
while cells with reduced Zn/Zn-MT levels were more susceptible to this treatment. H2O2
treatment resulted in oxidation on MT thiolate groups and loss of its metal binding
capacity with translocation of Zn released from oxidized MT to other cellular sites.
Preincubation of Ehrlich cells with ZnZO4 in vitro also conferred some degree of
resistance to H2O2 toxicity, suggesting the inherent antioxidative property of Zn ions.
These data suggested that Zn-MT can be considered as an antioxidant by virtue of its
thiolate groups and its Zn ions that are released in the presence of oxidative stress.
3. Anandh Babu PV., Sabitha KE., Shyamaladevi CS (No. 66 (Old No. 62) II Main Road,
Gandhi Nagar, Adayar, Chennai 600020, India): Therapeutic effect of green tea
extract on oxidative stress in aorta and heart of streptozotocin diabetic rats. Chem
Biol Interact, 162(2), 2006, 114-120. [40 Ref]

 Hyperglycemia induced oxidative stress has been proposed as cause of many
complications of diabetes including cardiac dysfunction. The present study depicts the
therapeutic effect of green tea extract on oxidative stress in aorta as well as heart of
streptozotocin diabetic rats. Six weeks after diabetes induction, green tea was
administered orally for 4 weeks [300 mg (kg body weight)-1 day-1]. In aorta and heart of
diabetic rats there was a significant increase in the activity of superoxide dismutase,
catalase and glutathione peroxidase with an increase in lipid peroxides. Diabetic rats
showed a significant decrease in the levels of serum and cardiac glutathione. Green tea
administration to diabetic rats reduced lipid peroxides and activity of antioxidant
enzymes whereas increased glutathione content. The results demonstrate that the
induction of antioxidant enzymes in diabetic rats is not efficient and sufficient to reduce
the oxidative stress. But green tea by providing a competent antioxidative mechanism
ameliorates the oxidative stress in the aorta and heart of diabetic rats. The study suggests
that green tea may provide a useful therapeutic option in the reversal of oxidative stress
induced cardiac dysfunction in diabetes mellitus.

4. Babu PVA., Sabitha KE., Shyamaladevi CS (Department of Biochemistry, University
of Madras, Guindy Campus, Chennai 600025, Tamilnadu, India): Green tea impedes
dyslipidemia, lipid peroxidation, protein glycation and ameliorates Ca2+-ATPase
and Na+/K+-ATPase activity in the heart of streptozotocin-diabetic rats. Chem Biol
Interact, 162(2), 2006, 157-164. [47 Ref]

 Diabetes-induced hyperlipidemia, oxidative stress and protein glycation impair cellular
calcium and sodium homeostasis associated with abnormal membrane-bound enzyme
activities resulting in cardiac dysfunction in biabetes. To explore the cardioprotective
mechanism of green tea in diabetes, we measured the changes in the levels of calcium,
sodium, potassium and the activities of Na+/K+-ATPase and Ca2+ ATPase in green tea
treated diabetic rat hearts. The effect of green tea on triglycerides, lipid peroxidation and
protein glycation in diabetic heart were also measured to elucidate the underlying
mechanisms. Diabetes was induced by streptozotocin (STZ, 60 mg/kg i.p.). Six weeks
after the induction of diabetes, some of the diabetic rats were treated orally with green tea
extract (GTE) (300 mg/kg/day) for 4 weeks. GTE produced reduction in blood glucose
and lowered the levels of lipid peroxides, triglycerides and extent of protein glycation in
the heart of diabetic rats. GTE blunted the rise in cardiac [Ca2+] and [Na+] whereas
increased the activities of Ca2+ ATPase and Na+/K+ ATPase in diabetic rats. In
conclusion, the data provide support to the therapeutic effect of GTE and suggest that a
possible mechanism of action may be associated with the attenuation of the rise in [Ca2+]
and [Na+] by ameliorating Ca2+-ATPase and Na+/K+-ATPase activities.
5. Devipriya S., Ganapathy V., Shyamaladevi CS (New No. 66, Second Main Road,
Gandhinagar, Adyar, Chennai 600025, India): Suppression of tumor growth and
invasion in 9, 10 dimethyl benz(a) anthracene induced mammary carcinoma by the
plant bioflavonoid quercetin. Chem Biol Interact, 162(2), 2006, 106-113. [48 Ref]

 Administration of qurecetin, a common polyphenolic component of many vascular and
edible plants including vegetables, fruits and tea significantly reduced the tumor volume
in rats induced for mammary carcinoma using dimethyl benz (a) anthracene (DMBA).
Dose response was assessed, by treating the animals with different doses (15-45 mg/kg
bw) of quercetin and 25 mg/kg bw was taken as effective dose. Quercetin was
administered as an intra tumoral injection once a week for 4 weeks. Serum levels of
carcino embryonic antigen (CEA), a potent marker for tumor growth and invasion was
significantly decreased on quercetin treatment. Quercetin caused a significant decrease in
the activities of acid phosphatase and Cathepsin D in serum of experimental animals.
Activities of lysosomal enzymes (B-D galactosidase, B-D glucuronidase, B-D
glucosidase and sialidase), in serum and tissue were significantly altered in DMBA
animals compared to control animals. However, quercetin treatment caused no significant
change in lysosomal enzyme activities in tissues, whereas the activities were significantly
lowered in serum. Partial purification of tissue type plasminogen activator (t-PA) from
the tumor and kidney showed increased activity in the DMBA induced animals. Serum
urokinase, -like plasminogen activator (u-PA) was also increased in animals with tumor,
indicating tumor invasion. Administration of quercetin caused a significant decrease of
both t-PA and u-PA. In conclusion, the present study suggests the possible role of
quercetin in primary and invasive mammary tumor treatment. The above observations in
vivo warrant further studies, due to the easy availability, common occurrence and low
toxicity of this dietary bioflavonoid.

6. Ognjanovic BI., Markovic SD., Pavlovic SZ (Institute of Biology and Ecology, Faculty
of Science, University of Kragujevac, Radoja Domanovica 12, P.O. Box 60,34000
Kragujevac, Serbia and Montenegro, Combined effects of coenzymes Q10 and vitamin
E in calcium induced alterations of antioxidant defense system in the rat heart.
Environ Toxicol Pharmacol, 22(2), 2006, 219-224. [47 Ref]

 Our study investigated the possible protective effects of coenzyme Q10 (CoQ10) and
vitamin E (Vit E) alone or in combination against cadmium (Cd) induced alterations of
antioxidant defense system in the rat heart. Male Wistar rats were injected with a single
dose of CdCl2 (0.4 mg Cd/kg BW i.p.), CoQ10 ( 20mg CoQ10/kg BW i.m.) and Vit E
(20 IU VitE/kg BW i.m.), alone or in combination. Acute intoxication of rats with Cd
were followed by significantly increased activity of antioxidant defense enzymes (CuZn
SOD, GSH-Px, GST and GR), while the activity of Mn SOD was decreased in the heart.
The treatment with Cd significantly decreased Vit C and Vit E concentrations. Treatment
with CoQ10 and VitE reversed Cd-induced alterations of antioxidant defense system. The
obtained results support the assumption that CoQ10 and Vit E function cooperatively
with endogenous antioxidants and diminished toxic effects of Cd in rat heart.
7. Pardini RS (Department of Biochemistry, University of Nevada, Rano, NV 89557,
USA): Nutritional intervention with omega-3 fatty acids enhances tumor response
to anti-neoplastic agents. Chem Biol Interact, 162(2), 2006, 89-105. [89 Ref]

 Nutritional intervention with specific fatty acids depresses tumor growth and enhances
tumor responsiveness to chemotherapy. Supplementation of tumors with long chained
omega-3 polyunsaturated fatty acids results in enrichment of tumor phospholipid
fractions with omega-3 fatty acids resulting in an altered membrane composition and
function. Tumors enriched with long chained omega-3 polyunsaturated fatty acids
possess membranes with increased fluidity, an elevated unsaturation index, enhanced
transport capabilities that results in accumulation of selective anti-cancer agents,
increased activity of selected drug activating enzymes, and alteration of signaling
pathways important for cancer progression. These nutritionally induced changes in tumor
fatty acid composition result in increased sensitivity to chemotherapy, especially in tumor
lines that are resistant to chemotherapy and cause specific enhancement of cytotoxicity to
tumor cells and protection of normal cells. Pre-disposing tumors to increased chemo-
sensitivity through nutritional intervention with specific fatty acids has the potential to
improve patient response to chemotherapy with fewer untoward side effects if these- pre-
clinical findings carry over into a clinical setting.

8. Srinivasan P., Sabitha KE., Shyamaladevi CS* (New No. 66, Old No. 62, II Main
Road, Gandhi Nagar, Adyar, Chennai 600020, India): Modulatory efficacy of green tea
polyphenols on glycoconjugates and immunological markers in 4-nitroquinoline 1-
oxide-induced oral carcinogenesis-A therapeutic approach. Chem Biol Interact,
162(2), 2006, 149-156. [47 Ref]

 Green tea polyphenols (GTP) has been used as a chemopreventive agent world wide
against chemically induced cancer. The present study is aimed to understand the
therapeutic action of GTP on glycoconjugates and immunological markers in 4-
Nitroquinoline 1-oxide (4-NQO)-induced oral cancer over a period of 30 days at 200
mg/kg, p.o., Oral cancer was induced by painting 4-NQO for 8 weeks followed by
administration of GTP after 22 weeks, for 30 days. Glycoconjugates such as hexose,
hexosamine, sialicacid, fucose and mucoprotein were analysed. Expression of
glycoconjugates was examined through histology and SDS-PAGE. Immunological
markers such as circulating immune complex and mast cell density were studied. Oral
cancer-induced animals showed a significant increase in levels of glycoconjugates and its
expression, similar to that observed for immunological markers. Treatment with GTP
altered the expression of glycoconjugates as well as immunological markers. The results
suggest that GTP modulates both the expression of glycoconjugates and immunological
markers resulting in regression of oral cancer.

To top