Alleviation of oxidative and nitrosative stress following curative resection in patient with oral cavity cancer.

BACKGROUND: Oxidative stress by reactive oxygen species (ROS) and nitrosative stress by reactive nitrogen species (RNS) are proven initiators and promoters in carcinogenesis. Elevated ROS/RNS with lowered antioxidants occur in patients with squamous cell carcinoma of oral cavity. Ours is the first study to evaluate the effect of curative resection on both oxidative and nitrosative stress in such patients. METHODS: This study was conducted on 24 cancer patients and with age- and sex-matched healthy controls. Lipid peroxidation products, nitric oxide (NO) products and ceruloplasmin (CPL) in plasma were measured before and after surgery. Similarly enzymatic antioxidants in erythrocytes and non-enzymatic antioxidants in plasma were measured. RESULTS: Statistically significant elevation of lipid peroxidation, NO products and CPL and depletion of antioxidants were found in cancer patients compared with controls. After curative surgical resection there was a statistically significant fall in oxidants and CPL coupled with a rise in antioxidants. CONCLUSIONS: Our results suggest that oxidative/nitrosative stress could play a significant role in oral cavity cancer (OCC) and that curative resection is effective in alleviating this oxidative/nitrosative burden. Significant mitigation of oxidative/nitrosative stress could indicate the completeness of resection since tumor forms the major source of oxidants.

Evidence of oxidative and nitrosative stress in patients with cervical squamous cell carcinoma.

BACKGROUND: We conducted a study to evaluate reactive oxygen species (ROS) and reactive nitrogen species (RNS) simultaneously together with the antioxidant status in patients with cervical carcinoma. METHODS: We measured lipid peroxidation product, including malondialdehye (MDA), nitric oxide (NO) products, including nitrite (NO(2)(-)), nitrate (NO(3)(-)) and total nitrite (TNO(2)(-)) and antioxidant enzymes in 45 patients with cervical cancer and compared them against 30 healthy controls. RESULTS: Plasma as well as erythrocyte MDA and plasma NO levels was higher (p<0.001) in cervical cancer as compared to healthy controls. Antioxidant enzymes, Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities, were decreased (p<0.001) whereas glutathione S-transferase (GST) activity was increased (p<0.001) in cervical cancer patients. Lipid peroxidation and NO products accumulation correlated significantly with a deranged antioxidant system. CONCLUSIONS: We demonstrated a possible involvement of both oxidative and nitrosative stress, as evidenced by increased lipid peroxidation and NO levels with altered antioxidant defense system in the pathogenesis of cervical cancer.

Enhanced lipid peroxidation and nitric oxide products with deranged antioxidant status in patients with head and neck squamous cell carcinoma.

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) can function both as initiators and promoters in carcinogenesis. Antioxidants provide protection against cellular and molecular damage caused by ROS and RNS. We conducted a study to evaluate the levels of lipid peroxidation products, nitric oxide (NO) products and antioxidants in patients with head and neck squamous cell carcinoma (HNSCC). Fifty one HNSCC patients, 33 healthy tobacco smokers/chewers as tobacco user controls, and 37 non-smokers/chewers as normal controls were recruited for this study. Lipid peroxidation products, NO products and antioxidants were measured using spectrophotometric methods. Lipid peroxidation products, including lipid hydroperoxide (LHP) and malondialdehyde (MDA), nitric oxide (NO) products, including nitrite (NO(2)(-)), nitrate (NO(3)(-)), and total nitrite (TNO(2)(-)) were found to be significantly elevated with a concomitant depletion of antioxidants in HNSCC patients as compared to tobacco users and normal controls. These derangements were also evident albeit to a lesser degree in tobacco users as compared to normal controls. Results from this study demonstrate a potential involvement of both ROS and RNS in the pathogenesis of HNSCC and also illustrate the risk of ROS/RNS induced damage healthy tobacco users are exposed to, implicating their higher risk for upper aerodigestive tract cancer.