Effect of gallic acid on renal biochemical alterations in male Wistar rats induced by ferric nitriloacetic acid.
The present study is an effort to identify a potent chemopreventive agent against various diseases (including cancer) in which oxidative stress and cell proliferation plays an important causative role. This study was designed to investigate the effect of gallic acid against ferric nitrilotriacetic acid (Fe-NTA)-induced carcinogen/ drug metabolizing phase I and phase II enzymes, antioxidative parameters, kidney markers, tumour promotion markers and lipid peroxidation (LPO) in kidney of male Wistar rats. Fe-NTA (9 mg Fe/kg body weight, intraperitoneally) caused significant depletion in the detoxification and antioxidant enzyme armoury with concomitant elevation in renal LPO, serum creatinine, blood urea nitrogen, hydrogen peroxide generation, ornithine decarboxylase activity and [3H]thymidine incorporation into renal DNA. However, pretreatment of animals with gallic acid (10 and 20 mg/kg body weight) resulted in a significant decrease in the levels of the parameters measured (P <0.001). Renal glutathione content (P <0.001), glutathione metabolizing enzyme (P <0.001) and antioxidant enzyme levels were also recovered to a significant level (P <0.001). The enhanced reduced glutathione level and enzyme activities involved in xenobiotic metabolism and maintaining antioxidant status of cells are suggestive of a chemopreventive efficacy of gallic acid against Fe-NTA-mediated oxidative stress, toxicity and cell proliferative response in Wistar rats.
Prasad
Lakshmi
L
Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi 110062, India.
Khan
Tajdar Husain
TH
Jahangir
Tamanna
T
Sultana
Sarwat
S
D000704:Analysis of Variance; D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D002273:Carcinogens; D018890:Chemoprevention; D004247:DNA / Q000378:metabolism; D004790:Enzyme Induction / Q000187:drug effects; D005290:Ferric Compounds; D005707:Gallic Acid / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000187:drug effects / Q000378:metabolism; D005982:Glutathione Transferase / Q000187:drug effects / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology; D007674:Kidney Diseases / Q000139:chemically induced / Q000517:prevention & control; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009571:Nitrilotriacetic Acid / Q000031:analogs & derivatives; D009955:Ornithine Decarboxylase / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric
D016588:Anticarcinogenic Agents; D002273:Carcinogens; D005290:Ferric Compounds; D005707:Gallic Acid; D004247:DNA; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D009955:Ornithine Decarboxylase; D005978:Glutathione; D009571:Nitrilotriacetic Acid; C020326:ferric nitrilotriacetate