AIMS: Evidence shows that diabetic patients may be predisposed to oxidative stress owing to increased glyco-oxidation and lipid peroxidation processes in consequence of chronic hyperglycemia. However, there is dearth of information whether glycemic control positively affects the antioxidant defense system in type 2 diabetes mellitus (T2DM). We investigated the potential association between glycemic control and oxidative stress biomarkers in controlled and uncontrolled diabetic states. METHODS: After obtaining ethical clearance, we included patients receiving metformin with glycated hemoglobin A1c ˂7.0% (glycemic control); newly diagnosed T2DM patients without glycemic control with hemoglobin A1c ˃7.0%; and apparently healthy normoglycemic individuals. The following biomarkers were determined: fasting glycemia level, malondialdehyde, glutathione peroxidase activity, catalase activity, total antioxidant capacity and total cholesterol level. The comparisons between the groups were made by ANOVA. RESULTS: The participants were 260 in number: 80 with controlled diabetes, 80 uncontrolled and 100 controls. All participants were between 40 and 71 years old. Fasting glycemia level and hemoglobin A1c showed significant reductions (p<0.05) in controlled T2DM against the uncontrolled T2DM group, all the same both were significantly higher (p<0.05) against the controls. Likewise, malondialdehyde levels showed significant elevations (p<0.05) correspondingly in both uncontrolled and controlled T2DM against the controls, accompanied with significant reductions (p<0.05) in the antioxidative enzyme activities (glutathione peroxidase activity and catalase activity) and total antioxidant capacity levels against the controls. In addition, total cholesterol was significantly reduced (p<0.05) in controlled T2DM against both uncontrolled T2DM and controls, respectively. There were significant correlations between hemoglobin A1c and oxidative stress biomarkers (p<0.05). CONCLUSION: There was no remarkable difference in oxidative stress states between glycemic controlled and uncontrolled T2DM, despite differences in their fasting glycemia and glycated hemoglobin levels. Our data, therefore, suggest that chronic hyperglycemia and possibly anti-diabetic medicationmay both equally associate with oxidative stress.

Background: In low-and middle-income countries, high burden of cervical cancer is associated with human papillomavirus (HPV) due to poor screening and diagnostic methods at early stage. Reports showed that there are discrepancies in data correlating HPV-infection with development of cervical cancer while the functional roles of P53  oncogenic mutation are controversial. Furthermore, the molecular pathogenesis of multiple HPV-genotypes remains an open question. Thus, advancing investigations on HPV-associated cervical abnormalities would add to early diagnostic precision. Methods: Two hundred (n=200) cervical samples were collected from apparently healthy, active adult women following an ethical approval. Laboratory analyses were conducted through cytological assessment and histochemistry screening using the Papanicolaou smear. PCR methods were used to characterize HPV-DNA genotypes and P53  gene mutations. Positive cervical dysplasia cases were matched with HPV-DNA, and the HPV-genotypes were used to evaluate the prevalence of various HPV-subtypes and the risk of cervical cancer. Results:  Twenty-four (n=24) cervical dysplasia and fifty-one (n=51) HPV+ were identified comprising single and multiple genotypes. While nine cases (n=9) showed p53  gene mutation with concurrent multiple high-risk HPV (hrHPV) genotypes, none of the single hrHPV genotypes had p53  mutation. More so, individuals with coexisting p53  mutation and multiple hrHPV-genotypes already manifesting cervical dysplasia were 22.2% of the group, while 77.8% had normal cervical architecture, the fate of whom was unknown during investigation. There was a higher cervical dysplasia among those with HPV oncogenes; there were connections between the HPV positivity with some genotypes (hrHPV16,18,31 and 33, respectively) and p53 mutation. Conclusion: P53 gene mutation was independent of HPV-associated cervical abnormalities in single hrHPV-genotype, though other mechanistic drivers attributed to p53 dysfunction by E6 and E7 remain plausible. On the other hand, infection with multiple hrHPVs showed a concomitant predominance with the P53  mutation, implying a potential interplay and an increased risk of cervical cancer.