Salivary superoxide dismutase levels in oral leukoplakia and oral squamous cell carcinoma; a clinicopathological study

Abstract

In the SouthEast Asian countries oral cancer is one among the commonly occurring malignancies due to tobacco use and quid chewing habits. Early stage diagnosis of the disease is reported to have a better prognosis. Sialochemistry studies involving antioxidants have recently gained importance as biomarkers for oral cancer risk assessment. The aim of this study was to estimate the levels of superoxide dismutase in saliva of patients with oral cancer, oral leukoplakia and healthy controls. Three study groups comprising of 25 oral cancer patients, 25 oral leukoplakia patients and 25 healthy controls were involved in the study. Saliva sample collected from the patients were evaluated superoxide dismutase by nitroblue tetrazolium (NBT) chloride method. The data obtained were analyzed using the one way ANOVA test. There was a significant difference between the levels of salivary superoxide dismutase in between oral cancer, oral leukoplakia groups when compared to healthy controls. The levels of salivary superoxide dismutase were significantly lower in oral cancer when compared to oral leukoplakia. These results suggest that salivary superoxide dismutase level estimation could be used to determine the risk of oral cancer as a non-invasive modality.

Utility Of Salivary CA-125 And LDH As Tumor Markers In Oral Malignancy

“…Shpitzer et al [28] and Shpitzer et al [31] also found total salivary LDH levels to be high in oral cancer patients. Our results are also comparable with the study done by Shetty et al [32] who have reported consistently higher salivary LDH levels in oral precancer and cancer patients as compared to healthy controls.…”

Lactate Dehydrogenase as a Tumor Marker in Oral Cancer and Oral Potentially Malignant Disorders: A Biochemical Study

“…The comparison of salivary LDH levels between oral cancer and healthy subjects was statistically significant (p < 0.001). Our study finding was in agreement with the study done by Kallalli et al, 1 Lokesh et al, 8 Shetty et al, 16 Patel and Metgud, 4 and Joshi et al…”

“…The comparison of salivary LDH levels between OSMF and healthy subjects was statistically significant (p < 0.001). Our study findings were consistent with the study conducted by Sivaramakrishnan et al, 3 Kallalli et al, 1 Bhambal et al, 2 Shetty et al, 16 Rathore et al, 9 Pereira et al, 6 and Muralidhar et al 14 According to WHO 2005, oral leukoplakia is defined as a predominantly white patch or plaque that cannot be characterized clinically or pathologically as any other disorder; oral leukoplakia carries an increased risk of cancer development either in or close to the area of leukoplakia or elsewhere in the oral cavity or the head and neck region. 17 Malignant transformation rate of oral leukoplakia varies from 0.13 to 34%.…”

“…18 In our study, there was a significant difference in the salivary and serum LDH levels between oral leukoplakia and healthy controls (p = 0.001). Our results were in accordance with the study conducted by Patel and Metgud, 4 Pereira et al, 6 Rathore et al, 9 Joshi et al, 11 Shetty et al, 16 and Achalli et al 19 In our present study, while comparing among all the study groups, we found that serum and salivary LDH levels were significantly higher in oral cancer followed by OSMF and oral leukoplakia. Intergroup comparison for mean value of salivary LDH levels was significantly higher in oral cancer group than control, oral leukoplakia, and OSMF groups (p < 0.0001).…”

Evaluation of salivary and serum lipid peroxidation, and glutathione in oral leukoplakia and oral squamous cell carcinoma

“…The enzymatic component includes superoxide dismutase (SOD), peroxidase, catalase (CAT), GST and GPx, while the nonenzymatic component includes uric acid and GSH (43 (44). Enzymes such as SOD are the most effective, intracellular, tumor-suppressing antioxidant enzyme that catalyzes the dismutation of oxygenated free radicals to less-reactive species, and therefore regulates cellular redox state and leads to tumor growth retardation (45). Peroxidase, CAT or GPx prevents carcinogenesis by converting H 2 O 2 produced by SOD into non-harmful molecular oxygen and water (34).…”