Hematological changes produced in mice by ochratoxin A

Gupta, Malaya; Bandopadhyay, Sumitra; Paul, Barnali; Majumder, Sayani

doi:10.1016/0300-483x(79)90095-7

Cited by 26 publications

(11 citation statements)

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“…Increase in ESR and hypercoagulability are correlated to the alterations of plasma proteins and coagulating factor(s), respectively. 29,30) The icteric condition of the animals is attributed to the hepatic dysfunctioning where more bile pigments may be produced. 31) Significant elevation in blood urea nitrogen and decrease in serum proteins seems related to the observed kidney damage.…”

Section: Discussionmentioning

confidence: 99%

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Sharma

Iqbal

2005

Biological & Pharmaceutical Bulletin

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The effect of long-term lithium treatment on renal function has been a matter of concern for about a quarter of centaury and remains controversial. For the last five decades researchers have been paying much attention to the lithium salts due to their therapeutic uses in controlling a variety of neurotic and psychosomatic manic depressions, neurotoxicity, affecting muricidal behavior and lithium sickness. [1][2][3][4] Extensive usage of lithium and its compounds in pharmaceuticals, dehumidifying and air conditioning units, ceramics and metallurgical processes, lubricants and in a number of chemical and biological laboratories brings this lightest alkali metal in close contact of human.Toxicity of lithium may be caused while taken as medicine. 5,6) Lithium salts cause ocular side effects, 7) polyuria, polydipsia, loss of body mass 8) and impaired renal concentration capacity after water deprivation.9) Lithium salts used as medicine can readily cross the placental barriers and produce teratogenic effects and toxicity. 10) In early pregnancy, lithium salt therapy elicited to be associated with a several fold increase in the incidence of cardiovascular anomalies in newborn, including tricuspid valve abnormalities.11) Cerebellar atropic changes related to lithium therapy 12) and peri-follicular inflammation and follicular plugging 13) even with the therapeutic limit of lithium level of blood have been observed. The occurrences of choreoathetosis 14) and abnormalities in lung and respiratory tract have also been reported by intake of lithium.15) Hypochromic microcytic anemia, hypercholesterolaemia, hyperglycemia, glycogenolysis, disturbance in TCA cycle and stimulation in transamination reaction in liver and kidney following repeated intramuscular injections of lithium nitrate in laboratory animals have been reported previously. 16,17) Renal insufficiency in long term lithium treatment has also been reported recently.18) This is an endeavor to study the histopathological and biochemical impacts of intake of small doses of lithium nitrate on renal tissue along with some blood parameters in male albino rats. Our results suggest that small doses of lithium induces toxicity in rats and therefore, studies evaluating its long-term tolerability are important. MATERIALS AND METHODS ChemicalsLithium nitrate, sodium citrate, diethylbarbiturate, 3,5-dinitrosalicilate, ammonium molybdate, citric acid, diacetylmonoxime, b sodium glycero phosphate, a ketoglutarate, a L-alaline, L-aspartate, sodium hypochlorite, trichloroacetic acid, and dinitrophenyl hydrazine were purchased from Sigma Chemical Company (St Louis, MO, U.S.A.). All other chemicals and reagent used were either of analytical grade or of highest purity, commercially available.Animals and Treatments Animals experiments were approved by animal care committee of Jamia Hamdard, care and handling of animals were in accordance with Indian Council of Medical Research guidelines. Male albino wistar rats (4-6 weeks) weighing 125-150 g, from Jamia Hamdard Central Animal House Col...

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Section: Discussionmentioning

confidence: 99%

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Sharma

Iqbal

2005

Biological & Pharmaceutical Bulletin

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“…The carcinogenic molecular mechanisms of OTA are based on the formation of DNA adducts or epigenetic changes (Fusi et al, 2010;Kocic et al, 2014). Several epigenetic mechanisms including protein synthesis inhibition, oxidative stress, alterations of cell signaling pathways and apoptosis in cell lines have been reported for OTA carcinogenicity (Gupta et al, 1979;Pfohl-Leszkowicz & Manderville, 2007;Salminen et al, 2010). A tolerable daily intake of 5 ng/kg b.w.…”

Section: Introductionmentioning

confidence: 99%

“…Ochratoxin A (OTA), a mycotoxin produced by several Aspergillus and Penicillium species, is classified as a group 2B carcinogen (Limonciel & Jennings, 2014) by the International Agency for Research on Cancer. Ingestion of OTA-contaminated feed or food has been associated with nephrotoxic Pfohl-Leszkowicz & Manderville, 2012), genotoxic (Gupta, Bandopadhyay, Paul, & Majumder, 1979) and carcinogenic (Pfohl-Leszkowicz & Manderville, 2007) effects, and perturbation of normal blood coagulation (Hassan et al, 2012) and immune response (Marin-Kuan, Cavin, Delatour, & Schilter, 2008). The carcinogenic molecular mechanisms of OTA are based on the formation of DNA adducts or epigenetic changes (Fusi et al, 2010;Kocic et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Honey and quercetin reduce ochratoxin A-induced DNA damage in the liver and the kidney through the modulation of intestinal microflora

Oršolić

Jembrek

Terzić

2017

Food and Agricultural Immunology

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This study was conducted to evaluate the interactions between the gut microbiota, ochratoxin A and functional food such as honey and quercetin, and the consequences of these interactions on ochratoxin-induced DNA damage in blood, liver and kidney cells. Honey (2 g kg −1 ) or Quercetin (50 mg kg −1 ) was applied to mice by intragastric application every day for 15 days, immediately before ochratoxin treatment (100 µg kg −1 ). We investigated colonic probiotic bacteria count, β-glucuronidase activity, the alkaline comet assay in blood, liver and kidney, the number of cells in the peritoneal cavity, macrophage spreading index and hematological and biochemical parameters. Honey and QU may reduce ochratoxin-induced DNA damage in the liver and kidney, β-glucuronidase activity and inflammation, partly through increasing the colon Bifidobacteria and Lactobacilli counts. The obtained results suggest that honey and QU counteracted the OTA-induced toxicity due to their bifidogenic activity and antigenotoxic activity. ARTICLE HISTORY

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“…OTA has been shown to induce a tubulointerstitial nephropathy in animals (Krogh et al, 1974) and enzymuria (Kane et al, 1986a,b) similar to Balkan endemic nephropathy found in humans (Krogh, 1992;Krogh et al, 1974;Petkova-Bocharova et al, 1988). In addition to nephrotoxicity, OTA disrupts blood coagulation (Galtier et al, 1979;Gupta et al, 1979) and glucose metabolism (Pitout, 1968). It is immunosuppressive (Creppy et al, 1983b;Haubeck et al, 1981;Lea et al, 1989;Stormer and Lea, 1995), teratogenic (Arora et al, 1983;Fukui et al, 1992;Szczech and Hood, 1981) and genotoxic (Creppy et al, 1985;Pfohl-Leszkowicz et al, 1991).…”

Section: Introductionmentioning

confidence: 94%

Brain's DNA Repair Response to Neurotoxicants

Sanchez‐Ramos¹

2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY) 01-07-2005 REPORT TYPE Annual DATES COVERED (From -To PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Florida Tampa, FL 33620 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTESOriginal contains color plates: All DTIC reproductions will be in black and white. ABSTRACTParkinson's Disease (PD) is associated with death of dopaminergic (DA) neurons in the substantia nigra (SN) of the brain. Military personnel abroad are at a greater risk of exposure to pesticides and toxins which may selectively damage DA neurons in the SN and increase the probability of development of Parkinson's disease (PD) later in life. The toxins of interest are mitochondrial poisons that create a bioenergetic crisis and generate toxic oxyradicals which damage macromolecules, including DNA. We hypothesize that regulation of the DNA repair response within certain neurons of the SN (the pars compacta) may be a critical determinant for their vulnerability to these neurotoxicants. We have measured regional differences in the brain's capacity to increase repair of oxidized DNA (indicated by oxyguanosine glycosylase (OGG1) activity) to three distinct chemical classes of neurotoxins (MPTP, two mycotoxins, and an organochloriine pesticide). At the end of the second year of the project, we have found that the temporal and spatial profile of OGG1 activity across brain regions elicted by each class of neurotoxicant is distinct and unique. Although all three toxicants cause DA depletion in striatum, only MPTP caused loss of DA neurons in midbrain. However, it is possible that superimposition of age-related loss of DA neurons over the moderate DS depletion caused by OTA may result in early onset parkinsonism. SUBJECT TERMSNo subject terms provided. REPAIR RESPONSES ELICITED BY MYCOTOXINS (OCHRATOXIN-A, RUBRATOXIN), ORGANOC...

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Hematological changes produced in mice by ochratoxin A

Cited by 26 publications

References 5 publications

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Lithium Induced Toxicity in Rats: A Hematological, Biochemical and Histopathological Study

Honey and quercetin reduce ochratoxin A-induced DNA damage in the liver and the kidney through the modulation of intestinal microflora

Brain's DNA Repair Response to Neurotoxicants

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