Possible action mechanism for curcumin in pre-cancerous lesions based on serum and salivary markers of oxidative stress.
Extensive research within the past half-century has indicated that curcumin (diferuloylmethane), a yellow pigment in curry powder, exhibits anti-oxidant, anti-inflammatory, and pro-apoptotic activities. We investigated whether the anti-pre-cancer activities assigned to curcumin are mediated through an anti-oxidant and DNA-protecting mechanism. Patients with oral leukoplakia, oral submucous fibrosis or lichen planus, and healthy individuals (n = 25 for each group) aged 17-50 years were selected. Salivary and serum oxidative markers such as malonaldehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), vitamins C and E were measured just prior to the intake of curcumin, after one week of curcumin intake and following clinical cure of precancerous lesions. Serum and salivary vitamins C and E showed increases, while MDA and 8-OHdG levels showed decreases in patients with oral leukoplakia, submucous fibrosis and lichen planus after intake of curcumin for all categories of precancerous lesions. The changes in these values were observed to be statistically significant after clinical cure of the disease (P < 0.05). The five-point rating scale for pain, as well as lesion size in oral leukoplakia, submucous fibrosis and lichen planus, improved significantly (P < 0.05). In addition, in submucous fibrosis, mouth opening (P < 0.05) recovered significantly. In oral leukoplakia, submucous fibrosis and lichen planus, the levels of serum and salivary vitamins C and E increased significantly, while MDA and 8-OHdG levels decreased after 131(15), 211(17), and 191(18) days, respectively. Values for serum and salivary vitamins C and E showed a significant decrease in oral leukoplakia, submucous fibrosis and lichen planus, in contrast to healthy individuals, but increased significantly in all groups subsequent to curcumin administration after clinical cure of lesions. Based on these results, we can conclude that curcumin mediates its anti-pre-cancer activities by increasing levels of vitamins C and E, and preventing lipid peroxidation and DNA damage.
Rai
Balwant
B
School of Dentistry, Oral Pathology and Maxillofacial Surgery, Catholic University Leuven, Leuven, Belgium. drdalwantraissct@rediffmail.com
Kaur
Jasdeep
J
Jacobs
Reinhilde
R
Singh
Jaipaul
J
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000293:Adolescent; D000328:Adult; D000975:Antioxidants / Q000032:analysis / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000032:analysis / Q000097:blood; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D003474:Curcumin / Q000627:therapeutic use*; D004247:DNA / Q000187:drug effects; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D006801:Humans; D007972:Leukoplakia, Oral / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D017676:Lichen Planus, Oral / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000097:blood; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D009914:Oral Submucous Fibrosis / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010147:Pain Measurement; D011230:Precancerous Conditions / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D020011:Protective Agents / Q000627:therapeutic use; D012463:Saliva / Q000737:chemistry*; D014810:Vitamin E / Q000032:analysis / Q000097:blood; D055815:Young Adult
D000975:Antioxidants; D015415:Biomarkers; D016166:Free Radical Scavengers; D020011:Protective Agents; D014810:Vitamin E; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D004247:DNA; D003849:Deoxyguanosine; D003474:Curcumin; D001205:Ascorbic Acid