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Open access

Saima Gul, Sagheer Ahmed, Humaira Gul, Kaneez Fatima Shad, Muhammad Zia-Ul-Haq and Diana Badiu

Abstract

Research on antioxidant potential from vegetables is increasingly focused on their effects on human health. However, relatively little work has been done to investigate the antioxidant effect of crude extract and/or different fractions from Brassica rapa L. In the present study, the antioxidant potential of crude extract and its fractions from Brassica rapa L. fruit part was tested for glutathione peroxidase (GPx), superoxide dismutase (SOD) enzymes and total antioxidant status (TAS) in blood samples. Our results reveal the fact that crude extract and each analyzed fraction (i.e. aqueous, ethyl acetate and chloroform) showed a concentration dependent effects on GPx, SOD and TAS in respect with saline solution (0.9% NaCl) used as negative control and vitamin C, as positive control. Therefore, GPx levels showed a highest value in crude extract and chloroform fraction (6981 U/L both at 10 mg/ml), SOD levels showed the same results in aqueous and ethyl acetate fractions (220 U/ml both at 10 mg/ml) and TAS in crude extract and all three fractions (i.e. aqueous, ethyl acetate and chloroform, 1.68 mmol/L at 10 mg/ml for all three fractions) in respect with saline solution (p<0.05). Furthermore, vitamin C showed the highest values on all three analyzed enzymes (8769 U/L for GPx, 223 U/ml for SOD and 1.8 mmol/L for TAS at 100 μg/ml). Our investigations have been proved to be promising in terms of future potential applications of crude extract and its fractions as components in a range of phytochemicals composition and/or different pharmaceutical usage, owing to their antioxidant potential.

Open access

Traian Vasile Constantin, Victor Lucian Mădan, Maria-Magdalena Constantin, Silviu-Horia Morariu and Bogdan Braticevici

Abstract

Prostate cancer is, after lung cancer, the most common malignant disease diagnosed in the male population. The introduction into the practice used during the 80’s and 90’s of the determination of serum Prostate-Specific Antigen (PSA) levels, as a component of screening for prostate cancer, was a turning point in the medical practice. Due to this enzyme produced exclusively by the prostate gland, the prostate cancer detection rate (in curative, intracapsular stages) improved significantly. Serum PSA is a better predictive factor for prostate cancer (PC) than digital rectal examination or transrectal prostatic ultrasound.

Open access

Aleksandar Arsenijevic, Jelena Milovanovic, Bojana Stojanovic, Marija Milovanovic, Eric M. Gershwin, Patrick Leung, Nebojsa Arsenijevic and Miodrag L. Lukic

Abstract

Primary biliary cirrhosis (PBC) is an autoimmune disease of the liver that is, characterised by destruction of the intrahepatic bile ducts and the presence of antimitochondrial antibodies (AMAs). Several murine models of PBC, with similar serological, biochemical, and histological features to human PBC, have been developed in recent years. These animal models enable investigators to study the etiology and pathophysiologic mechanism of PBC. Immune response in PBC is directed towards E2 components of the 2-oxo-acid dehydrogenase family of enzymes, which is in located in mitochondria and is an immunodominant epitope (a lipoylated peptide sequence shared by enzymes). Immunisation of mice with 2-octynoic acid coupled to bovine serum albumin (2-OA-BSA) (which is an antigen that is structurally related to the E2 subunit of the pyruvate dehydrogenase complex [PDC-E2]) produces histologic features similar to those found in human PBC. Th is model of xenobiotic induced PBC is suitable for studying the early events in PBC pathogenesis and for developing new therapeutics in PBC.

Open access

Aleksandra Nikolić-Kokić, Zorana Oreščanin-Dušić, Marija Slavić, Ivan Spasojević, Zorica Stević, Mihajlo Spasić and Duško Blagojević

Summary

Background: Mutated copper, zinc-containing superoxide dismutase (SOD1) may self-aggregate, an event that could also be an initial cause of motor neuron malfunction leading to disease onset. The effects of human mutated SOD1 pro- tein from the blood of familial amyotrophic lateral sclerosis (FALS) patients bearing Leu144Phe (L144F) mutation were compared to wild-type (WT) human SOD1 derived from healthy examinees, for enzymatic activity and the effects on isometric contractions of non-vascular smooth muscle.

Methods: We isolated WT and L144F SOD1 enzymes from eight patients with FALS, L144F mutation in exon 5 and eight healthy controls. We then investigated SOD1 activities in the obtained samples by the adrenaline method and pro- filed them electrophoretically. Finally, we applied WT and L144F SOD1 on the isolated rat uterus.

Results: L144F SOD1 showed lower superoxide-dismutating activity compared to WT human SOD1. We found that, in contrast to WT human SOD1, mutated L144F does not induce smooth muscle relaxation.

Conclusions: Our data suggest that the lack of relaxation of muscle tonus in the presence of mutated SOD1 may have pathogenic feedback effects in FALS.

Open access

Lorena Ciumărnean, Ştefan C. Vesa, Eleonora Dronca, Dorel P. Sâmpelean, Vasile C. Vlad, Maria S. Moldovan and Cadariu A. Achimaş

Abstract

Study objective. The objective of this study was to investigate PON1 phenotype and genotype in Romanian patients with abdominal obesity. Materials and methods. The study groups consisted of 88 patients with abdominal obesity and 46 subjects with normal waist circumference, matched for age and gender. For each patient, we determined the clinical parameters that may influence PON1 activities. Q192R and L55M polymorphisms analysis in the PON1 gene were performed by PCR-RFLP using specific primers and restriction enzymes. PON1 lactonase, paraoxonase and arylesterase activities were assayed by spectrophotometric methods. Analysis of PON1 genotypes and activities distribution in the obese and non-obese individuals was performed with Med- Calc Software (Version 12.4.0.0). Results. There was no statistically significant difference between obese and controls in regards to age and gender. The study revealed that PON1 activities were not influenced by gender. Of all PON1 activities, only the paraoxonase activity was inversely correlated with age, being significantly reduced in patients with abdominal obesity compared to non-obesity (p=0.009). Abdominal circumference independently influenced only the variation of arylesterase activity (R2=6.5%, p=0.003). Distribution of PON1 genotypes in the study groups was significantly different (p=0.007) only for the Q192R but not for the L55M genotypes. The QR genotype had the highest influence on paraoxonase activity (R2=40.6; p<0.001). The MM genotype had the greatest influence on arylesterase (R2=11.3%, p<0.001) and lactonase activities (R2=7.4%, p<0.001). Conclusions. Q192R genotypes distribution was significantly different in obese patients and the QR genotype influenced greatly the paraoxonase activity. The MM genotype had the most important independent influence on the lactonase and arylesterase activities .

Open access

Ivan Kosalec, Snježana Ramić, Dubravko Jelić, Roberto Antolović, Stjepan Pepeljnjak and Nevenka Kopjar

Assessment of Tryptophol Genotoxicity in Four Cell Lines In Vitro: A Pilot Study with Alkaline Comet Assay

Tryptophol is an aromatic alcohol and secondary metabolite of the opportunistic fungus Candida albicans. Although its toxicity profile at cell level has been poorly investigated, recent data point to cytotoxic, cytostatic, and genotoxic effects in lymphocytes and the induction of apoptosis in leukaemic blood monocytes. In this pilot study we evaluated the genotoxicity of tryptophol in vitro on four permanent cell lines of animal and human origin: ovary cells, alveolar epithelium, liver cells, and blood monocytes using the alkaline comet assay. We selected cells that might be principal targets of tryptophol and other low-molecular geno(toxins) secreted by Candida albicans during host invasion. Our results suggest that tryptophol applied in vitro at 2 mmol L-1 for 24 h damages DNA in HepG2, A549 and THP-1 cells, obviously due to bioactivation and/or decomposition of the parent compound, which results in the formation of more genotoxic compound(s) and production of reactive species that additionally damage DNA. On the other hand, notably lower levels of primary DNA damage were recorded in CHO cells, which lack metabolic activity. Future studies with tryptophol should look further into mechanisms involved in its toxic action and should focus on other cell types prone to infection with Candida spp. such as vaginal epithelial cells or keratinocytes of human origin.

Open access

Uriel Bachrach

SUMMARY

The naturally occurring polyamines, spermine, spermidine and the diamine putrescine are widespread in nature. They have been implicated in growth and differentiation processes. In 1967, we reported that cancer cells are rich in polyamines. Subsequently, it has been shown that polyamines are released from cancer cells and may be detected in body fluids such as urine, blood and cerebrospinal fluids. It has also been demonstrated that the increase in cellular polyamine levels is an early and an obligatory event in the process of malignant transformation. This increase in cellular polyamine concentration is due to the activation of ornithine decarboxylase (ODC), which catalyses the rate limiting step in polyamine synthesis by converting ornithine to putrescine. Assays of urinary and blood polyamines have been used to detect cancer and to determine the success of therapy. A sensitive, rapid, chemiluminescence-based method for the determination of diamines and polyamines was developed and 2.000 urine samples were tested. An interesting "gene therapy" system for injecting amine oxidases into normal and transformed cells was developed as follows: serum amine oxidase and porcine kidney damine oxidase were trapped within reconstituted Sendai virus envelopes. Chick or rat fibroblasts, transformed by Rous sarcoma virus, were more susceptible to the injected enzymes, compared to the normal culture, when macromolecular synthesis was tested. An in vitro chemosensitivity assay for the testing of the sensitivity of cancer cells from individual patients ("tailored treatment") was also developed. All these studies stress the importance of polyamines in carcinogenesis.

Open access

Jovana Trbojevic, Jadranka Odovic, Jasna Trbojevic-Stankovic, Biljana Stojimirovic and Ratomir Jelic

REFERENCES 1. Lemke TL, Williams DA (eds). The Foye’s Principles of Medicinal Chemistry 6 th ed. Wolters Kluwer, Lippincott Williams & Wilkins, Philadelphia, 2013. 2. Giverhaug T, Falck A, Eriksen BO. Effectiveness of anti-hypertensive treatment in chronic renal failure: to what extent and with which drugs do patients treated by nephrologists achieve the recommended blood pressure? J Hum Hypertens 2004; 18: 649-54. 3. Piepho RW. Overview of the angiotensin-convering-enzime inhibitors. Am J HealthSystem Pharm 2000; 57: 3-7. 4. Rang HP

Open access

Milivoj Dopsaj and Jelena Ivanović

-132. Dopsaj, M., Milošević, M., Blagojević, M. (2000). An analysis of the reliability and factoral validity of selected muscle force mechanical characteristics during isometric multi-joint test. In Proceedings of the XVIII International Symposium of Biomechanics in Sport , 25-30 June, 2000. Hong Kong, China: Chinese University, Department of Sports Science and Physical Education, 146-149. Komi, P.V., Karlsson, J. (1978). Skeletal muscle fibre types, enzime activities and physical performance in young males and females. Acta Physiologica

Open access

Nikolina Babić

Summary

The term »personalized medicine« (PM) was coined in the late 1990s, but was not introduced to general US public until about a decade later, through Genomics and Personalized Medicine Act. According to this act, PM is defined as any clinical practice model that utilizes genomic and family history information to customize diagnostic and therapeutic interventions and improve health outcomes. One of the emerging disciplines essential for implementation of PM is clinical pharmacogenomics (PGx), where patient’s genetic information is utilized to personalize drug therapy. PGx testing includes mostly detection of small DNA variations, such single nucleotide polymorphisms (SNPs), insertions, and deletions in the genes encoding the drug transporters, receptors and metabolizing enzymes. By providing the right drug at the optimal dose to each patient, PGx promises to significantly improve drug efficacy and prevent adverse drug reactions. In the early 2000s, the US Food and Drug Administration joined scientists and laboratorians in their efforts to translate recent genetic advances into clinical practice by requiring the drug manufacturers to include genetic information on their product labels. To date several drugs including irinotecan, warfarin, abacavir and clopidogrel are labeled with the information relating different enzymatic polymorphisms with the adverse drug effects or the impaired drug efficacy. The majority of PGx testing involves SNP detection within the family of Cytochrome (CYP) P450 enzymes responsible for metabolism of most drugs, such as anti-depressants (e.g. CYP2D6) and anticoagulants (e.g. CYP2C9, 2C19) to name a few. PGx tests are still very low volume tests and it is not clear how and to what extent genotyping information is being utilized in the clinical practice, mostly due to the lack of outcome studies demonstrating the clinical utility of PGx testing. For instance, it is well known that approximately 30% of Caucasian population carries a polymorphic CYP2C9 allele that predisposes them to higher warfarin sensitivity and thus to increased bleeding risk. How - ever, there are no large, randomized outcome studies that conclusively demonstrate reduction of bleeding events or decrease in hospitalization rates in population dosed based on genotype information. The clinicians are thus reluctant to incorporate warfarin genotyping into their practice. Despite the attention PGx has received in recent years, the adoption of PGx into routine clinical testing is still far from being commonplace. The barriers to wider adoption and implementation of PGx include lack of education and understanding by prescribing physicians regarding the available tests, lack of consensus guidelines on interpretation and use of genotype results and scarcity of randomized controlled trials demonstrating the clinical utility of PGx testing. However, as ge netic testing is becoming increasingly patient driven thought di - rect-to-consumer testing, clinicians and laboratorians must continue to work toward full implementation of PGx testing into routine clinical practice.