Oxidative Stress Markers in Intestinal Mucosa of Tunisian Inflammatory Bowel Disease Patients

Background/Aims:

Inflammatory bowel diseases (IBDs), Crohn''s disease (CrD) and ulcerative colitis (UC), are chronic gastrointestinal inflammatory disorders. The precise etiology of IBD remains unclear, and it is thought that interactions among various factors, including, genetic factors, the host immune system and environmental factors, cause disruption of intestinal homeostasis, leading to dysregulated inflammatory responses of the gut. As inflammation is intimately related to formation of reactive intermediates, including, reactive oxygen species, oxidative stress has been proposed as a mechanism underlying the pathophysiology of IBD. The purpose of this study is to examine the lipid peroxidation, protein oxidation and anti-oxidative profile in Tunisian IBD.

Materials and Methods:

Malondialdehyde (MDA), conjugated dienes (CD), protein thiol levels, as well as the catalase (CAT) activity were evaluated in intestinal biopsies of 17 patients affected by IBD (12 CrD and 5 UC) and 12 healthy control individuals.

Results:

Oxidative stress was confirmed in these two types of disease biopsies as compared to controls. MDA and CD levels were significantly increased in both UC and CrD patients’ biopsies as compared to controls’ biopsies (P < 0.001). CAT activity was similar in UC and CrD biopsies’ and was not significantly increased in IBD patients’ biopsies compared with controls’ biopsies (P > 0.05). Anon-significant decrease in thiol (SH) level was observed in both UC and CrD patients’ biopsies compared with controls’ biopsies (P > 0.05).

Conclusion:

Increased levels of MDA and CD in IBD patients’ biopsies underline the implication of oxidative stress in the physiopathology of IBD.     

A comparative study of oxidant–antioxidant status in stable and active vitiligo patients

The pathogenetic mechanisms in vitiligo have not been completely clarified. One of the major hypotheses in the pathogenesis of vitiligo is the oxidative stress hypothesis. The active or stable phase of vitiligo is defined on the basis of the progression or appearance of new lesions in the last 3 months and the absence of new lesions or their progression in the last 6 months, respectively. Eighteen patients with active vitiligo, 18 patients with stable vitiligo, and 40 controls were included in this study. We examined serum levels of malondialdehyde, selenium, vitamin E and A, and the erythrocyte activities of glutathione peroxidase, superoxide dismutase, and catalase. Our results revealed a significantly higher level of serum malondialdehyde, selenium in patients with active disease compared with the controls. Significant higher increase in erythrocytes superoxide dismutase activities was observed in active vitiligo group, erythrocyte glutathione peroxidase activity was decreased significantly in active disease, whereas erythrocyte catalase activity and plasma vitamin E and A levels were not different in vitiligo patients as compared with controls. Our study shows that oxidative stress is involved in the pathophysiology of both active and stable vitiligo but increased imbalance of antioxidants was observed in the blood of active vitiligo patients.I dedicate this article to our dear director (Mme Hentati Basma) who dead in 06/06/06. We will never forget you and you are always in our heart.     

The paraoxonase L55M and Q192R gene polymorphisms and myocardial infarction in a Tunisian population

ObjectivesIn the present study, we examined a possible association between the PON1 Q192R and L55M polymorphisms and myocardial infarction (MI) in a sample of the Tunisian population.Design and methodsThree hundred and ten patients with MI and 375 controls were recruited. Paraoxonase gene polymorphisms at codon 192 and 55 were analyzed by PCR-RFLP.ResultsGenotype distributions and allele frequencies of L55M were similar among the control and MI groups. For the Q192R polymorphism patients with MI had significantly higher frequency of the RR genotype compared to controls [17.1% vs. 10.9%; OR (95% CI), 1.93 (1.24–3.02); p = 0.004]. The MI patient group showed a significantly higher frequency of the R allele compared to the controls [38% vs. 30%; χ² = 10.74, p = 0.001]. The association between the PON1 Q192R polymorphism and MI remained significant after adjustment for other well-established cardiovascular risk factors.ConclusionsThe present study showed a significant and independent association between the PON1 Q192R polymorphism (presence of R allele) and MI in the Tunisian population.     

Clinicopathologic significance of DNA methyltransferase 1, 3a, and 3b overexpression in Tunisian breast cancers

DNA methyltransferase 1, 3a, and 3b affect DNA methylation, and it is thought that they play an important role in the malignant transformation of various cancers. The current study was designed to analyze DNA methyltransferase expression by immunohistochemistry in a series of 94 Tunisian sporadic breast carcinomas. Results were correlated to clinicopathologic parameters and promoter methylation status of 8 tumor suppressor genes (BRCA1, BRCA2, RASSFA1, TIMP3, CDH1, P16, RARβ2, and DAPK). Overexpression of DNA methyltransferase 1, 3a, and 3b was detected in 46.8%, 32%, and 44.7% of cases, respectively. A significant correlation was found between DNA methyltransferase 1 overexpression and Scarff-Bloom-Richardson histologic grade III (P = .01). DNA methyltransferase 3a overexpression was significantly associated with menopausal status (P = .01), Scarff-Bloom-Richardson histologic grade III (P = .0001), estrogen (P = .04) and progesterone (P = .007) receptor negativity, and HER2 overexpression (P = .004). However, DNA methyltransferase 3a overexpression was found less frequently in the luminal A intrinsic breast cancer subtype (9.7%) than in luminal B (53%), HER2 (41%), and triple-negative (50%) subtypes (P = .001). DNA methyltransferase 3b overexpression shows significant correlation with promoter hypermethylation of BRCA1 (P = .03) and RASSFA1 (P = .04) and with the hypermethylator phenotype (more than 4 methylated genes, P = .01). These data suggest that overexpression of various DNA methyltransferases might represent a critical event responsible for the epigenetic inactivation of multiple tumor suppressor genes, leading to the development of aggressive forms of sporadic breast cancer.     

Recent advances in research on radiofrequency fields and health: 2001-2003

The widespread use of wireless telecommunications devices, particularly mobile phones, has resulted in increased human exposure to radiofrequency (RF) fields. Although national and international agencies have established safety guidelines for exposure to RF fields, concerns remain about the potential for adverse health outcomes to occur in relation to RF field exposure. The extensive literature on RF fields and health has been reviewed by a number of authorities, including the Royal Society of Canada (1999), the European Commission's Scientific Committee on Toxicity, Ecotoxicity, and the Environment (CSTEE, 2001), the British Medical Association (2001), the Swedish Radiation Protection Authority (Boice & McLaughlin, 2002), and the Health Council of The Netherlands (2002). This report provides an update on recent research results on the potential health risks of RF fields since the publication of the Royal Society of Canada report in 1999 (See Krewski et al., 2001a) and our previous 2001 update (Krewski et al., 2001b), covering the period 2001-2003. The present report examines new data on dosimetry and exposure assessment, biological effects such as enzyme induction, and toxicological effects, including genotoxicity, carcinogenicity, and testicular and reproductive outcomes. Epidemiological studies of mobile phone users and occupationally exposed populations are examined, along with human and animal studies of neurological and behavioral effects. All of the authoritative reviews completed within the last 2 yr have concluded that there is no clear evidence of adverse health effects associated with RF fields. However, following a recent review of nine epidemiological studies of mobile phones and cancer, Kundi et al. (2004) concluded that the possibility of an enhanced cancer risk cannot be excluded. These same reviews support the need for further research to clarify the possible associations between RF fields and adverse health outcomes that have appeared in some reports. The results of the ongoing World Health Organization (WHO) study of mobile phones will provide important new information in this regard.     

Polymorphisms in the CC-chemokine receptor-2 (CCR2) and -5 (CCR5) genes and risk of myocardial infarction among Tunisian male patients

ObjectivesThe aim of the present study was to investigate the association between CCR2-Val64Ile and CCR5-Δ32 variants and the estimation of haplotypes with MI in a sample of the Tunisian population.Design and methodsA total of 290 unrelated MI patients and 282 healthy controls were studied. The CCR2-Val64Ile and CCR5-Δ32 variants were analyzed by PCR-RFLP.ResultsSubjects carrying at least one copy of the CCR5-deletion allele were significantly more common in the control group, suggesting an atheroprotective effect (adjusted OR = 0.44, 95% CI = 0.28–0.72, p = 0.001). Haplotype analysis showed that MI patients had significantly less 64Val-Del haplotype (9.9% vs. 21.3%, OR = 0.30, 95% CI = 0.21–0.43, p < 0.001) and 64Ile-Ins haplotype (12.3% vs. 16.7%, OR = 0.58, 95% CI = 0.42–0.80, p < 0.001).ConclusionA protective effect of the CCR5-Δ32 polymorphism against MI in the Tunisian population was found.     

Towards nationwide control of schistosomiasis in Yemen: a pilot project to expand treatment to the whole community

Both the urinary and intestinal forms of schistosomiasis are thought to be widespread in the Republic of Yemen, with estimates of 3 million people infected and 600 000 suffering clinical morbidity. Sub-national control has been ongoing since 2006 via the distribution of praziquantel (PZQ) against schistosomiasis and albendazole (ALB) against soil-transmitted helminths using school-based treatment. In preparation for a 6-year nationwide control programme with the aim of expanding treatment to the wider community, a new programmatic approach of complementing school-based distribution with community-based treatment was trialled in 10 highly endemic districts in three governorates in December 2009. The new approach achieved coverage of 90.1% of non-enrolled children: a 40% increase compared with the same districts in 2008, and coverage of 97.9% of enrolled children: a 2% increase compared to 2008. Coverage of females (children and adults) was 81.8%, and of adults in general was 73.9%. The total cost per person treated was US$0.66 (US$0.79 in 2008), which includes training, health education, social mobilization, distribution and drugs. These results provide hope that a combined school and community-based approach can be successfully implemented on a wider scale during the main control programme in 2010-2015, with approximately 10 million people targeted in the first year alone.