Antidotes/Treatment/Detoxification 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' (44.5mg/100g). 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.
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