Premila Abraham

ORCID: 0000-0003-0467-0733
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Research Areas
  • Chemotherapy-induced organ toxicity mitigation
  • Acute Lymphoblastic Leukemia research
  • Childhood Cancer Survivors' Quality of Life
  • Drug-Induced Hepatotoxicity and Protection
  • HIV/AIDS drug development and treatment
  • Biotin and Related Studies
  • Pharmacological Effects and Toxicity Studies
  • Oral health in cancer treatment
  • Polyomavirus and related diseases
  • Neurological Complications and Syndromes
  • Liver Disease and Transplantation
  • Alcohol Consumption and Health Effects
  • Metabolism and Genetic Disorders
  • HIV Research and Treatment
  • Sulfur Compounds in Biology
  • Tryptophan and brain disorders
  • Eicosanoids and Hypertension Pharmacology
  • Liver Disease Diagnosis and Treatment
  • Vitamin K Research Studies
  • Biomedical Research and Pathophysiology
  • Alcoholism and Thiamine Deficiency
  • Muscle and Compartmental Disorders
  • Vitamin D Research Studies
  • Gestational Diabetes Research and Management
  • Birth, Development, and Health

Christian Medical College, Vellore
2013-2025

Christian Medical College
2010-2023

Centre Hospitalier Universitaire d'Angers
2013

University of Arizona
2009

Brigham and Women's Hospital
2000

University Medical Center New Orleans
1999

Louisiana State University
1999

<i>Background:</i> Nephrotoxicity is one of the adverse side effects methotrexate (MTX) chemotherapy. The mechanism renotoxicity MTX not fully understood. It essential to understand nephrotoxicity in order diminish and hence maximize benefits <i>Objectives:</i> aim study was verify whether oxidative stress neutrophil infiltration play a role MTX-induced renal damage using rat model. <i>Methods:</i> Adult male rats were administered at dose 7 mg/kg body...

10.1159/000192391 article EN Chemotherapy 2009-01-01

Abstract Nephrotoxicity is an adverse side effect of methotrexate (MTX) chemotherapy. The present study verifies whether melatonin, endogenous antioxidant prevents MTX‐induced renal damage. Adult rats were administered 7 mg/kg body weight MTX intraperitoneally for 3 days. In the melatonin pretreated rats, 40 mg/ kg was daily 1 h before administration MTX. killed 12 after final dose MTX/vehicle. kidneys used light microscopic and biochemical studies. markers oxidative stress measured along...

10.1002/cbf.1676 article EN Cell Biochemistry and Function 2010-06-29

Nephrotoxicity is a dose limiting side effect of tenofovir, reverse transcriptase inhibitor that used for the treatment HIV infection. The mechanism tenofovir nephrotoxicity not clear. Tenofovir specifically toxic to proximal convoluted tubules and tubular mitochondria are targets cytotoxicity. Damaged major sources reactive oxygen species cellular damage reported occur after antioxidants depleted. purpose study investigate alterations in antioxidant system induced renal using rat model....

10.1186/1423-0127-20-61 article EN cc-by Journal of Biomedical Science 2013-01-01

The efficacy of methotrexate (MTX), a widely used chemotherapeutic drug, is limited by its gastrointestinal toxicity and the mechanism which not clear. present study investigates possible role mitochondrial damage in MTX-induced enteritis. Small intestinal injury was induced Wistar rats administration 7 mg kg −1 body wt. MTX intraperitoneally for 3 consecutive days. resulted severe small extensive to enterocyte mitochondria. Respiratory control ratio, single most useful reliable test...

10.1177/0960327113515503 article EN Human & Experimental Toxicology 2013-12-17

The long-term use of tenofovir, a commonly used anti-HIV drug, can result in renal damage. mechanism tenofovir disoproxil fumarate (TDF) nephrotoxicity is not clear, although it has been shown to target proximal tubular mitochondria. In the present study, effects chronic TDF treatment on function, mitochondrial and activities electron transport chain (ETC) complexes were studied rats. Damage mitochondria dysfunction was observed. impaired function such as respiratory control ratio,...

10.1002/jbt.21560 article EN Journal of Biochemical and Molecular Toxicology 2014-03-10

Abstract: Gentamicin is an antibiotic that widely used against serious and life‐threatening gram‐negative infections. However, its clinical use limited by nephrotoxicity. Oxidative stress nitrosative are reported to play important role in gentamicin In the present study we investigated whether ebselen, inhibitor of oxidative prevents or reduces gentamicin‐induced renal damage rat. For this purpose male Wistar rats were divided into five groups treated as follows. Group 1 (control group):...

10.1111/j.1742-7843.2006.pto_474.x article EN Basic & Clinical Pharmacology & Toxicology 2006-08-23

Abstract Cyclophosphamide (CP) is an antineoplastic agent that used for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) a major dose limiting side effect CP. Recent studies show aminogaunidine, inhibitor inducible nitric oxide synthase potent antioxidant and prevents changes caused by oxidative stress such as depletion activity tissue injury. The purpose study to investigate aminoguanidine on parameters stress, enzymes bladder injury Adult male rats were randomly divided...

10.1002/cbf.1534 article EN Cell Biochemistry and Function 2008-12-23

Cyclophosphamide (CP) is widely used in the treatment of tumors and B-cell malignant disease, such as lymphoma, myeloma, chronic lymphocytic leukemia, Waldenstrom's macroglobulinemia. Renal damage one dose-limiting side effects CP. Oxidative stress reported to play important roles CP-induced renal damage.To find out whether aminoguanidine (AG) protects against oxidative damage.Renal was induced rats by administration a single injection CP at dose 150 mg/kg body weight intraperitoneally. For...

10.1179/174329211x12968219310837 article EN Redox Report 2011-01-01

The incidence of endometrial cancer is increasing globally. Cancer stem cells are now considered the driving force for tumour recurrence and metastasis. We studied whether proportion cell population stemness gene expression differ in type I II cancer. Type tissues were obtained from patients who underwent hysterectomy. tissue was digested using collagenase, we established a primary culture. In cultures these two types cancer, used flow cytometry to measure expressing CD 133 CXCR4 on its...

10.34763/jmotherandchild.20252901.d-24-00041 article EN PubMed 2025-02-01

10.1007/s10157-004-0335-6 article EN Clinical and Experimental Nephrology 2005-03-31

Nephrotoxicity is one of the adverse side effects cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim study was to verify whether glutamine, precursor for synthesis, prevents damage using rat model. Adult male rats were administered single dose 150 mg/ kg body weight CP intraperitoneally. glutamine-pretreated 1 gm/kg glutamine orally 2 h before administration CP....

10.1177/0960327110376552 article EN Human & Experimental Toxicology 2010-07-09

These studies test the hypothesis that acute and chronic alcohol intoxication stimulate release of oxygen-derived radicals in liver. Male Sprague-Dawley rats received an intravenous bolus followed by continuous infusion ethanol to maintain blood level at about 175 mg/dl for 0-18 hr. They were then allowed recover from this "alcohol binge" free during recovery phase was monitored. In model, fed with 40% agar blocks 16 weeks. Acute induced two phases hepatic superoxide release. The first...

10.2741/bautista article EN Frontiers in bioscience 1999-01-01

Electron microscopy was used to examine changes in the subcellular organelles of rat kidney at different time intervals after a single exposure cyclophosphamide (CP). The morphological were studied points (6 hrs, 16 hrs and 24 hrs) single-dose administration CP. Six rats killed each Saline-treated served as controls. CP resulted alterations various including peroxisomes, lysosomes, mitochondria, endoplasmic reticulum (ER) renal tubular epithelium well damage glomerulus. basement membrane...

10.1177/0960327111402240 article EN Human & Experimental Toxicology 2011-03-18
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