Summary
In a living donor kidney transplantation (LDKT) dominated transplant programme, kidney paired donation (KPD) may be a cost‐effective and valid alternative strategy to increase LDKT in ...countries with limited resources where deceased donation kidney transplantation (DDKT) is in the initial stages. Here, we report our experience of 300 single‐centre KPD transplantations to increase LDKT in India. Between January 2000 and July 2016, 3616 LDKT and 561 DDKT were performed at our transplantation centre, 300 (8.3%) using KPD. The reasons for joining KPD among transplanted patients were ABO incompatibility (n = 222), positive cross‐match (n = 59) and better matching (n = 19). A total of 124 two‐way (n = 248), 14 three‐way (n = 42), one four‐way (n = 4) and one six‐way exchange (n = 6) yielded 300 KPD transplants. Death‐censored graft and patient survival were 96% (n = 288) and 83.3% (n = 250), respectively. The mean serum creatinine was 1.3 mg/dl at a follow‐up of 3 ± 3 years. We credit the success of our KPD programme to maintaining a registry of incompatible pairs, counselling on KPD, a high‐volume LDKT programme and teamwork. KPD is legal, cost effective and rapidly growing for facilitating LDKT with incompatible donors. This study provides large‐scale evidence for the expansion of single‐centre LDKT via KPD when national programmes do not exist.
Many plant products are known to exert antioxidative effects by quenching various free radicals and singlet molecular oxygen. Andrographis paniculata (Kalmegh) is used extensively in the Indian ...traditional system of medicine as a hepatoprotective and hepatostimulative agent and has been reported to have antioxidant effects against different hepatotoxins. The present study aims to analyze antioxidant properties of an active component, andrographolide (ANDLE), extracted from A paniculata. This study investigates the effect of andrographolide on the hepatocellular antioxidant defense system and lipid peroxidation of control mice, mice treated with hexachlorocyclohexane (BHC) only, and andrographolide + BHC. Glutathione (GSH), glutathione-s-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSH-Px), γ-glutamyl transpeptidase (γ-GTP), superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation (LPO) are studied by spectrophotometric methods. The BHC experimental model forms an irreversible liver tumor in male mice. The activities of GSH, GR, GSH-Px, SOD, and CAT show significant (P
≤ .05) increases, while γ-GTP and GST show significant decreases (P
≤ .05) in andrographolide-supplemented mice as compared with BHC-treated mice. This study indicates that the antioxidant effect of andrographolide could be due to its ability to activate antioxidant enzymes that catalyze the reaction of oxidants and are effective in severe liver damage.
Relevance. The present investigation relates to the influence of andrographolide, an active compound of Andrographis paniculata Nees. It reverses an experimental liver carcinogenic condition of mice ...to normal and might be a potential therapeutic/preventive agent for human liver cancer. Objective. A. paniculata (Kalmegh) is extensively used in the Indian traditional system of medicine as a hepatoprotective and hepatostimulative agent and has been reported to have protective effect against different hepatotoxins. Materials and methods. Histomorphological, ultrastructural, and biochemical studies were performed for the effect of the andrographolide on control mice, mice treated with hexachlorocyclohexane (BHC) only and BHC + andrographolide. Enzymes for liver function tests were analyzed by spectrophotometric method. Results. The BHC experimental model forms an irreversible liver tumor in male mice. The histological and ultrastructural changes observed in andrographolide supplementation emphasize the recovery of the damaged liver. This recovery was also reflected in the neoplastic nodule formation. The activity of phosphorylase and glucose-6-phosphatase in the liver of the andrographolide-supplemented group suggests improved glycogenolysis in liver. Serum glutamate pyruvate transaminase, serum glutamate oxalate transaminase, alkaline phosphatase, acid phosphatase, and γ-glutamyl transpeptidase showed a significant decrease in andrographolide-supplemented animals as compared with BHC-treated animals, suggesting regenerative effects elicited by andrographolide. Conclusion. The study indicates that the regenerative capability elicited by andrographolide is possibly due to its ability to reactivate liver function enzymes that catalyze the reaction of several biochemical and synthetic processes and that it may be useful for severe liver damage conditions.
Oral cancer accounts third of all malignancies in India. Tobacco use, the major etiological factor for oral cancer is known to generate free radicals resulting in alterations in antioxidant enzymes ...like, glutathione-S-transferase (GST), glutathione reductase, superoxide dismutase, catalase, and glutathione peroxidase as well as lipid peroxidation and total thiol. Therefore, it is of fundamental importance to evaluate the role of tobacco and antioxidant enzymes and oxidative stress markers in oral carcinogenesis.
One hundred forty oral cancer patients and 50 healthy controls, classified as "habitual controls" and "nonhabitual controls" having tobacco habits and no tobacco habits, respectively, were included in the study. Adjacent normal and malignant tissue samples were also collected. Erythrocyte, plasma, and tissue levels of antioxidant enzymes and total thiol were assayed by spectrophotometric methods. GSTM1 genotype was analyzed using polymerase chain reaction.
Antioxidant enzymes were significantly higher whereas glutathione peroxidase and thiol levels were lower in patients as compared with habitual controls. Habitual controls with higher tobacco exposure and lower antioxidant enzymes as well as thiol showed higher risk of oral cancer development. Antioxidant enzymes were higher, whereas catalase and thiol levels were lower in malignant as compared with adjacent normal tissues. Sixty-three percent of the patients showed GSTM1 null genotype.
The study showed risk of oral cancer development in habitual controls with lower antioxidant enzymes, lower oxidative stress markers, and higher lifetime tobacco exposure. Individuals with GSTM1 null genotype may be at higher risk of oral cancer development.
Tobacco is the major etiological factor for oral cancer development through the generation of oxidative stress. Therefore, markers of oxidative stress such as total antioxidant status, lipid ...peroxidation, and total thiol levels might be useful to monitor oxidative stress and predict overall survival in oral cancer patients. The study included 140 oral cancer patients and 50 healthy controls, who were classified as with the habit of tobacco and no habit of tobacco. Adjacent normal and malignant tissue samples were collected from oral cancer patients. Plasma and tissue levels of lipid peroxidation, thiol, and total antioxidant status were assayed by spectrophotometric methods. Thiol levels were significantly lower in controls with the habit of tobacco (P
= .033), oral cancer patients ( P
= .0001), and malignant tissues (P
= .015) as compared to controls with no habit of tobacco, controls with the habit of tobacco, and adjacent normal tissues, respectively. Tobacco exposure was higher in oral cancer patients than controls with the habit of tobacco. Controls with the habit of tobacco who had lower thiol (odds ratio OR = 10.58, P
= .008) and high tobacco exposure (OR = 0.251, P
= .05) showed an elevated risk of oral cancer development. Patients showing a lipid peroxidation level above the cutoff level as compared to patients below the cutoff level showed poor overall survival, whereas those with thiol and total antioxidant status levels below the cutoff level as compared to their respective counterparts showed poor overall survival. In conclusion, lipid peroxidation and thiol could be useful for predicting the risk of oral carcinogenesis in healthy tobacco consumers and predicting overall survival of oral cancer patients.
Tobacco is a major etiological factor for oral cancer development, accounting 30-40% of all cancer cases in India. Tobacco consumption generates free radicals and causes oxidative damages. In order ...to counteract these lethal effects, normal living cells have multiple antioxidant defense systems in a cascade manner. Thus, it seems that studying biological parameters, like antioxidant enzyme system, may be helpful in risk assessment and early diagnosis of oral cancer. Therefore, we analyzed erythrocytic and tissue antioxidant enzyme activities in terms of glutathione-S-transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and plasma thiol levels.
Study included healthy controls with no habit of tobacco (NHT, n = 25), controls with habit of tobacco (WHT, n = 31) and oral cancer patients (n = 52). All the parameters were analyzed with highly sensitive and specific spectrophotometric methods.
Erythrocytic SOD and plasma thiol levels were significantly lower (p = 0.03), while GPx and CAT levels were higher (p = 0.017) in WHT as compared to NHT. No significant changes in GST and GR levels were observed between NHT and WHT. GST, GR, SOD and CAT activities were significantly higher (p = 0.05, p < 0.001, p = 0.003 and p < 0.001, respectively) while GPx and thiol levels were lower (p = 0.035 and p < 0.001, respectively) in oral cancer as compared to WHT. Odds ratio for erythrocytic GR, SOD, CAT and plasma thiol showed significantly higher risk of oral cancer development in WHT. Mean levels of SOD and CAT were increased, while GPx and thiol were decreased with the increase in habit duration in oral cancer. GST, GR and SOD activities were significantly higher (p = 0.0001, p = 0.005 and p = 0.005, respectively), while, CAT and thiol levels were lower (p = 0.0001 and p = 0.015, respectively) in malignant tissues as compared to adjacent normal tissues.
The data revealed that evaluation of antioxidant enzyme activities and thiol levels in WHT can be helpful to identify individuals at a higher risk of oral cancer development
To analyze chromosomal aberrations (CA) as an index of DNA damage, to measure DNA repair capability using mutagen sensitivity assay and to correlate tobacco exposure with CA.
Oral cancer patients, ...healthy tobacco chewers and healthy tobacco nonusers were studied for spontaneous and mutagen-induced CA. An arbitrary unit obtained for lifetime tobacco exposure (LTE) was compared with CA.
Mean levels of spontaneous and mitomycin-C-induced CA were higher in patients as compared to chewers and controls. DNA repair capability of patients was significantly deficient (p < or = 0.016) as compared to that of chewers. LTE was significantly higher (p = 0.004) in patients than chewers. Chewers having high LTE and spontaneous CA above cutoff levels might be at a greater risk of oral carcinogenesis.
There is a probable risk of oral carcinogenesis in healthy tobacco consumers having higher CA and LTE. Whether the deficient DNA repair capacity of oral cancer patients is due to the disease process or the tobacco exposure needs to be confirmed with a larger population study.
Background: Tobacco chewing is attributed to oral cancer. Prediction of cancer development by genotoxicity analysis is a major challenge to identify tobacco users at greater risk. Therefore, present ...study aimed to analyze tobacco related genotoxic effects in chewers monitoring micronuclei (MN) and chromosome aberrations (CA). The biomarkers were compared with non chewer to (i) predict risk for genotoxicity, (ii) estimate synergistic effect of tobacco exposure with level of biomarkers, and (iii) identify best cellular site of measurements for genotoxicity assessment. Methods: Healthy tobacco chewers (n=47); and controls (n=48) were enrolled in the study. The peripheral blood lymphocyte and exfoliated buccal mucosa cells were studied for CA and micro nucleated cell count (MNC) respectively. An arbitrary unit was obtained for Lifetime Tobacco Exposure (LTE) using frequency/day multiplied by duration of years of tobacco use. Data were analyzed using SPSS statistical software. Results: MNC was significantly higher (p=0.001) in chewers than controls. CA was higher in chewers than controls. MNC can differentiate higher tobacco exposure in chewers than CA. Controls having MNC above cutoff level have greater risk of genotoxic exposition (95% C.I.; 1.462-23.26, p=0.012). Conclusion: The present study concludes that MNC is a better surrogate biomarker to predict genotoxicity than CA for tobacco exposure and DNA damage index in tobacco chewers.
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