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Celecoxib, a selective cyclo-oxygenase-2 (Cox-2) inhibitor, prevents the formation of prostaglandins, responsible for maintenance of renal function. Celecoxib administration may lead to renal damage. Since free radicals and antioxidant mechanisms play a significant role in renal injury; this study was designed to evaluate the role of oxidative stress in celecoxib-induced renal damage. The administration of celecoxib resulted in moderate and mild tubulointerstitial nephritis in chronic and acute group. The renal function tests were significantly altered only in the chronic group. The results in both the acute and the chronic group showed (1) a significant increase in the lipid peroxidation and in the activities of superoxide dismutase, catalase and glutathione-S-transferase and (2) a decrease in nitrite, reactive thiols and glutathione. In conclusion, our study suggests that chronic administration of celecoxib may have a damaging effect on kidney, as evident through altered histopathology and renal functions. This damage may be mediated by oxidative stress.

OBJECTIVES: The intestinal permeability (IP) of sugars and their derivatives has been widely used to assess mucosal damage in gastrointestinal diseases. Ulcerative colitis (UC) is a recurring and relapsing disease that causes inflammation of the gut. IP of sugars can be evaluated and correlated with the flare of UC. MATERIALS AND METHODS: A prospective study was conducted on 91 patients with active UC at the tertiary care center in North India. Mayo grading system assessed disease activity, and IP was assessed by measuring sucrose, lactulose, mannitol, and sucralose in urine samples from UC patients. A high-performance liquid chromatography (HPLC) method to detect all of these sugars simultaneously using a refractive index detector was developed and further validated in patients with UC. RESULTS: The analytical recovery rate of the tested sugars ranged from 95% to 146% in the urine matrix. The limit of detection and limit of quantification were 78.838 mg/L and 262.79 mg/L for sucrose, 84.994 mg/L and 283.31 mg/L for lactulose, 74.789 mg/L and 249.30 mg/L for mannitol, and 50.908 mg/L and 169.69 mg/L for sucralose. CONCLUSION: The standardized HPLC method is sensitive and suitable for the simultaneous detection and determination of different sugar moieties in the urine sample. Patients with UC can be evaluated indirectly for the flare by estimating the recovery rate of sugars through gut permeability. The procedure is noninvasive and thus improves the quality of life of chronically ill patients.

Acute kidney injury (AKI) in severe acute pancreatitis (SAP) has a high mortality rate. Traditionally used serum creatinine is an insensitive biomarker for the early detection of AKI. We aimed to study the role of plasma and urinary neutrophil gelatinase-associated lipocalin (NGAL) in predicting AKI and a severe course in patients with acute pancreatitis (AP). Consecutive patients of AP who presented within 72 h of symptom onset and age- and gender-matched healthy controls were included. Urinary and serum NGAL levels [enzyme-linked immunosorbent assay (ELISA)] were evaluated within 24 h of and 72 h after admission and once in controls. Urine and serum NGAL levels were correlated with development of AKI, severity, and outcomes of AP. Fifty patients with AP and 30 controls were enrolled. The mean serum and urine NGAL levels in patients on day 1 were significantly higher than the serum and urine NGAL levels in controls (  < 0.001). After excluding patients with AKI on day 1 (  = 10), both serum and urinary NGAL levels on days 1 and 3 were significantly higher in patients who subsequently developed AKI (  = 11) compared to those who did not (  = 29) (  = 0.02, 0.01 and  < 0.001, 0.03). A urinary NGAL level of 221.03 ng/mL on day 1 predicted AKI with a sensitivity and specificity of 82 and 80%, respectively (AUC = 0.9). Mean serum and urinary NGAL levels on day 1 were significantly elevated in patients with SAP compared to those without SAP (  = 0.04 and <0.001). NGAL levels in urine and serum can predict severity of AP and development of AKI.

Fish oil (FO) rich in n-3 polyunsaturated fatty acids (PUFAs) have a protective role in autoimmune disorders, type 2 diabetes, rheumatoid arthritis, and cancer, whereas corn oil (CO) rich in n-6 PUFAs has a proinflammatory and procarcinogenic effect. A balanced n-3/n-6 PUFA ratio in diet rather than absolute intake of either may be responsible for decreasing cancer incidence. This study was designed to evaluate the chemopreventive effect of different ratios of FO and CO on prognostic markers, DNA damage, and cell cycle distribution in colon carcinogenesis. Male Wistar rats were divided into control, N,N′-dimethylhydrazine dihydrochloride (DMH) treated, FO+CO(1:1)+DMH, and FO+CO(2.5:1)+DMH. All the groups, except control, received a weekly injection of DMH for 4 weeks. The animals were given modified AIN-76A diets and killed either 48 h later (initiation phase) or kept for 16 weeks (postinitiation phase). The animals treated with DMH in both the phases showed an increase in multiple plaque lesions, total sialic acid, lipid associated sialic acid, DNA damage and cell proliferation. However, levels of p53 in the postinitiation and cyclin D1 in both the phases were significantly elevated. FO+CO(2.5:1)+DMH treatment in both the phases led to a decrease in multiple plaque lesions, DNA damage, total sialic acid, lipid associated sialic acid as compared with the DMH treated group. There was a G1 arrest with a decrease in p53 and cyclin D1 levels in FO+CO(2.5:1) in both the phases whereas treatment with FO+CO(1:1)+DMH led to same results in the postinitiation phase only. This study suggests that FO+CO(2.5:1) is more effective in chemoprevention of experimental colon carcinogenesis.

n-3 Polyunsaturated fatty acids (PUFA) have a chemopreventive effect while n-6 PUFA promote carcinogenesis. The effect of these essential fatty acids may be related to oxidative stress. Therefore, the study was designed to evaluate the effect of different ratios of fish oil (FO) and corn oil (CO) in the prevention of colon cancer. Male Wistar rats were divided into control, dimethylhydrazine dihydrochloride (DMH) treated, FO + CO (1:1) and FO + CO (2.5:1). All the groups, except the control received a weekly injection of DMH for 4 weeks. The animals were sacrificed either 48 h later (initiation phase) or kept for 16 weeks (post initiation phase). DMH treatment in the initiation phase animals showed mild to moderate inflammation, decreased ROS and TrxR activity, increased antioxidants, apoptosis and ACF multiplicity. The post initiation study showed severe inflammation with hyperplasia, increased ACF multiplicity and ROS levels, a decrease in antioxidants and apoptosis. The FO + CO (1:1) treated animals showed severe inflammation, a decrease in ROS, an increase in antioxidants and apoptosis in the initiation phase. FO + CO (1:1) in the post initiation phase and FO + CO (2.5:1) in the initiation showed mild inflammation, increased ROS, apoptosis and decreased antioxidants. There was a decrease in ACF multiplicity and ROS levels, increased antioxidants and apoptosis in the post initiation phase study. The present study suggests that FO has a dose- and time-dependent chemopreventive effect in colon cancer mediated through oxidative stress and apoptosis.

Cyclooxygenase-2 (COX-2) enzyme plays an important role in cancer development. COX-2 inhibition by non-steroidal anti-inflammatory drugs is a useful approach for cancer prevention, but its usage has been associated with side effects. n −3 polyunsaturated fatty acids also exhibit a chemopreventive effect mediated by COX-2 inhibition. Therefore, the present study was designed to evaluate the effect of combined dosage of celecoxib and fish oil in experimental mammary carcinogenesis. Female Wistar rats were distributed as control, 7,12-dimethyl benz(α)anthracene (DMBA) treated, celecoxib + fish oil (20 mg/kg b.w. + 0.5 ml), celecoxib + fish oil (30 mg/kg b.w. + 0.25 ml), and their corresponding controls treated with fish oil or celecoxib only. The treatment was given for 7 days, and on the 8th day animals of all the groups except the control group received DMBA orally and sacrificed after 90 days. The histopathology, DNA fragmentation, total sialic acid (TSA), lipid-associated sialic acid (LASA), and oxidative stress were measured in mammary tissue and liver mitochondrial fraction. The results showed ductal hyperplasia and an increase in TSA, LASA, lipid peroxidation, and nitrite levels with a decrease in the antioxidants on DMBA treatment. Pretreatment with celecoxib and fish oil in DMBA-treated animals led to normal histology, increase in DNA fragmentation, and decrease in TSA and LASA levels with reduced oxidative stress, and the effect was more pronounced than animals pretreated with either celecoxib/fish oil alone suggesting a synergistic effect of the two regimens. To conclude, a combination of celecoxib and fish oil is a better strategy for cancer chemoprevention than celecoxib/fish oil alone.