R. Kumaraguruparan

Antioxidant profile in the circulation of patients with fibroadenoma and adenocarcinoma of the breast

OBJECTIVES To correlate the extent of lipid peroxidation with the antioxidant status in the circulation of patients with fibroadenoma and adenocarcinoma of the breast. DESIGN AND METHODS Ten fibroadenoma and thirty breast cancer patients and an equal number of age- and sex- matched normal subjects were chosen for the study. Lipid peroxidation as evidenced by thiobarbituric acid reactive substances (TBARS) and the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST) ascorbic acid and vitamin E were estimated. RESULTS Enhanced lipid peroxidation with concomitant depletion of antioxidants was observed in breast cancer patients as compared to normal subjects and fibroadenoma patients (p < 0.05). A similar pattern of changes was seen in fibroadenoma patients as compared to corresponding normal subjects (p < 0.05). CONCLUSION This study has revealed an imbalance in the redox status in patients with fibroadenoma and adenocarcinoma of the breast.

Tissue lipid peroxidation and antioxidant status in patients with adenocarcinoma of the breast

BACKGROUND Carcinoma of the breast, the third most common cancer worldwide, accounts for the highest morbidity and mortality. The increasing global incidence of breast cancer emphasizes the need to understand the various mechanisms involved in breast tumorigenesis. The present study was undertaken to evaluate the use of lipid peroxidation and antioxidants as biomarkers in human mammary tumors. METHODS The extent of lipid peroxidation as evidenced by the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) as well as the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) in tumor tissues and adjacent normal tissues of 30 breast cancer patients was estimated. RESULTS Lipid peroxidation in breast cancer tissues was enhanced compared to the corresponding adjacent uninvolved tissues. This was accompanied by significant elevation in both enzymic and non-enzymic antioxidants. CONCLUSIONS We suggest that upregulation of antioxidants induced by oxidative stress confers a selective growth advantage to tumor cells over their adjacent normal counterparts.

Oxidant-antioxidant status in patients with oral squamous cell carcinomas at different intraoral sites

OBJECTIVES To compare the extent of lipid peroxidation and the status of antioxidants in tumor and venous blood of patients with oral squamous cell carcinoma (OSCC) at different intraoral sites. DESIGN AND METHODS Twenty four patients with OSCC at different intraoral sites and an equal number of age- and sex-matched reference subjects were chosen for the study. The concentrations of lipid peroxides and reduced glutathione (GSH) and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were estimated in tissues and blood. RESULTS Diminished lipid peroxidation in tumor tissue was accompanied by decreased activities of SOD and CAT with increase in GSH and GSH-dependent enzymes. In contrast, enhanced lipid peroxidation with decrease in antioxidants was observed in the venous blood of OSCC patients. CONCLUSION No significant differences in lipid peroxidation and antioxidant levels were observed between patients with OSCC at different intraoral sites. However, our results revealed differences between the tumor and blood with respect to their susceptibility to lipid peroxidation and antioxidant status.

Protective Effects of Ethanolic Neem Leaf Extract on N‐Methyl‐N′‐nitro‐N‐nitrosoguanidine‐Induced Genotoxicity and Oxidative Stress in Mice

We evaluated the effects of pretreatment with ethanolic neem leaf extract on N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG)‐induced genotoxicity and oxidative stress in male Swiss albino mice. The frequency of micronuclei (MN), concentrations of lipid peroxides and the status of the antioxidants, reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione‐S‐transferase (GST) were used as intermediate biomarkers of chemoprotection. Animals were divided into four groups of five animals each. Animals in group 1 were given MNNG (40 mg/kg body weight) by intragastric intubation. Animals in group 2 received intragastric administration of ethanolic neem leaf extract at a concentration of 200 mg/kg body weight for 5 days followed by MNNG 1.5 h after the final feeding. Group 3 animals received ethanolic neem leaf extract alone for five days. Group 4 received the same volume of normal saline and served as control. The animals were sacrificed by cervical dislocation 27 h after the carcinogen exposure. In MNNG‐treated mice, enhanced lipid peroxidation with compromised antioxidant defences in the stomach, liver and erythrocytes was accompanied by increase in bone marrow micronuclei. Pretreatment with ethanolic neem leaf extract significantly reduced MNNG‐induced micronuclei and lipid peroxides and enhanced GSH‐dependent antioxidant activities. The results of the present study demonstrate that ethanolic neem leaf extract exerts protective effects against MNNG‐induced genotoxicity and oxidative stress by augmenting host antioxidant defence mechanisms.

Altered oxidant-antioxidant profile in canine mammary tumours

Mammary tumours are the most common neoplasms in female dogs. Oxidative stress arising due to overproduction of reactive oxygen species, coupled with altered antioxidant capacities has been implicated in the pathogenesis of all types of cancers. However, the extent of lipid peroxidation and the status of antioxidants in canine mammary tumours have not been investigated. The present study was designed to evaluate the oxidant–antioxidant profile in canine mammary tumours. Lipid peroxidation as evidenced by the formation of thiobarbituric acid-reactive substances, lipid hydroperoxides, and conjugated dienes, as well as the status of the antioxidants superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, glutathione S-transferase and vitamin C, in tumour tissues of 25 bitches was estimated. Lipid peroxidation in tumour tissues was enhanced compared to the corresponding adjacent uninvolved tissues. This was accompanied by significant elevation in both enzymatic and non-enzymatic antioxidants. This study suggests that upregulation of antioxidants induced by lipid peroxidation confers a selective growth advantage to tumour cells over their adjacent normal counterparts.

Black tea polyphenols protect against 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis.

Dietary chemoprevention has emerged as a cost-effective approach for cancer control. We evaluated the chemopreventive effects of black tea polyphenols (Polyphenon-B) administration during the preinitiation phase of 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. The expression of proliferating cell nuclear antigen (PCNA) in the buccal pouch and the concentration of lipid peroxides, protein carbonyl, and the antioxidant status in the buccal pouch, liver and erythrocytes were used as biomarkers of chemoprevention. All the hamsters painted with DMBA alone for 14 weeks developed buccal pouch carcinomas associated with increased expression of PCNA, diminished lipid and protein oxidation, and enhanced antioxidant status. In the liver and erythrocytes of tumor-bearing animals, enhanced oxidation of lipids and proteins was accompanied by compromised antioxidant defenses. Dietary administration of Polyphenon-B effectively suppressed DMBA-induced HBP carcinogenesis as revealed by decreased incidence of tumours and PCNA expression. In addition, Polyphenon-B modulated lipid and protein oxidation and enhanced the antioxidant status in the pouch, liver, and erythrocytes. We suggest that Polyphenon-B exerts its chemopreventive effects by inhibiting cell proliferation in the target tissue and modulating the oxidant-antioxidant status in the target as well as in host tissues.

Protective Effects of Ethanolic Neem Leaf Extract on DMBA-Induced Genotoxicity and Oxidative Stress in Mice

We evaluated the effects of pretreatment with ethanolic neem leaf extract on 7,12-dimethylbenz[a]anthracene (DMBA)-induced genotoxicity and oxidative stress in male Swiss albino mice. The frequency of bone marrow micronuclei, the extent of hepatic lipid peroxi-dation and the status of antioxidants-reduced glutathione (GSH), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were used as intermediate biomarkers of chemoprotection. In DMBA-treated mice, the increases in micronuclei and lipid peroxides were accompanied by compromised antioxidant defenses. Pretreatment with ethanolic neem leaf extract (200 mg/kg body weight) significantly reduced DMBA-induced micronuclei and lipid peroxides and enhanced GSH-dependent antioxidant activities. The results of the present study suggest that ethanolic neem leaf extract exerts protective effects against DMBA-induced genotoxicity and oxidative stress by enhancing the antioxidant status.

Oxidant-Antioxidant Status in Oral Precancer and Oral Cancer Patients

The present investigation was undertaken to examine the blood levels of lipid peroxides and the antioxidants superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase, and glutathione-S-transferase in oral precancer, preoperative, postoperative, and recurrent oral cancer patients with age- and sex-matched normal healthy subjects as controls. In patients with oral precancer and oral cancer, enhanced lipid peroxidation was accompanied by antioxidant depletion. These changes were more pronounced in patients with recurrent oral tumors. Twelve weeks after surgery, decreased lipid peroxidation was accompanied by increased antioxidant levels. The results of this study indicate that imbalance in the redox status of oral cancer patients may be due to enhanced lipid peroxidation and compromised antioxidant defenses.

Garlic Oil Enhances Hepatic and Blood Antioxidants During Hamster Buccal Pouch Carcinogenesis

We analyzed the protective effect of garlic oil on hepatic and blood lipid peroxidation and the antioxidant status during buccal pouch carcinogenesis induced by 7,12-dimethylbenz[a]anthracene (DMBA) in male Syrian hamsters. Enhanced lipid peroxidation in the liver and blood of tumor-bearing animals was accompanied by a significant decrease in antioxidant levels. Topical application of garlic oil effectively suppressed oral carcinomas, decreased lipid peroxidation, and enhanced antioxidant levels. Our results suggest that garlic oil may exert its chemopreventive effects by modulating lipid peroxidation and enhancing antioxidant status in the liver and blood.