ABSTRACT
CONTEXT: Vanillin is known to possess important antioxidant activity. OBJECTIVE: The current study was conducted to establish the therapeutic efficiency of vanillin against potassium bromate (KBrO3)-induced depression-like behavior and oxidative stress in mice. MATERIAL AND METHODS: Mice were exposed during 15 days either to potassium bromate (KBrO3), KBrO3+ vanillin or to only vanillin. RESULTS: Our results revealed a significant modification in the fatty acid composition of the KBrO3-treated mice. In addition, KBrO3 induced a significant reduction in enzymatic activities and gene expressions, Na+ -K+ and Mg2+-ATPases, acetylcholinesterase and butylcholinesterase activities. The gene expression of tumor necrosis factor-α, interleukin-1ß, interleukin-6 and COX2, significantly increased in the cerebrum of KBrO3-treated group. Histopathological observations were consistent with these effects. Co-treatment with vanillin significantly attenuated KBrO3-induced oxidative stress and inflammation. CONCLUSION: This work suggests that vanillin mitigates KBrO3-induced depression, and that this neuroprotective effect proceeds through anti-oxidant and anti-inflammatory activities.
Subject(s)
Antioxidants/pharmacology , Benzaldehydes/pharmacology , Depression/prevention & control , Gene Expression Regulation/drug effects , Neuroprotective Agents/pharmacology , Neurotoxicity Syndromes/drug therapy , Animals , Behavior, Animal/drug effects , Bromates/toxicity , Butyrylcholinesterase/genetics , Butyrylcholinesterase/metabolism , Ca(2+) Mg(2+)-ATPase/genetics , Ca(2+) Mg(2+)-ATPase/metabolism , Cerebrum/drug effects , Cerebrum/metabolism , Cerebrum/physiopathology , Cyclooxygenase 2/genetics , Cyclooxygenase 2/metabolism , Depression/chemically induced , Depression/genetics , Depression/metabolism , Fatty Acids/metabolism , Glutathione Peroxidase/genetics , Glutathione Peroxidase/metabolism , Interleukin-1beta/genetics , Interleukin-1beta/metabolism , Interleukin-6/genetics , Interleukin-6/metabolism , Lipid Peroxidation/drug effects , Mice , Neurotoxicity Syndromes/genetics , Neurotoxicity Syndromes/metabolism , Neurotoxicity Syndromes/physiopathology , Oxidative Stress/drug effects , Protein Carbonylation/drug effects , Sodium-Potassium-Exchanging ATPase/genetics , Sodium-Potassium-Exchanging ATPase/metabolism , Superoxide Dismutase/genetics , Superoxide Dismutase/metabolism , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolismABSTRACT
The present study aimed to explore the ability of vanillin to ameliorate the adverse effects induced by potassium bromate (KBrO3) in the renal tissue. Our results showed a significant increase in hydrogen peroxide, superoxide anion, malondialdehyde, advanced oxidation protein product and protein carbonyl levels in the kidney of KBrO3 treated mice, compared with the control group. Nephrotoxicity was evidenced by a decrease in plasma uric acid and kidney glutathione levels, Na(+)-K(+)-ATPase, lactate dehydrogenase and catalase activities. Additionally, creatinine and urea levels significantly increased in the plasma and declined in the urine. Also, Kidney glutathione peroxidase, superoxide dismutase, metallothionein (MT1 and MT2) mRNA expression remarkably increased. These modifications in biochemical and molecular values were substantiated by histopathological data. Co-treatment with vanillin restored these parameters to near control values. Interestingly, vanillin proved to possess, in vitro, a stronger scavenging radical activity than vitamin C and Trolox. Thus, vanillin inhibited KBrO3-induced damage via its antioxidant and antiradical activities as well as its capacity to protect genes expression and histopathological changes.
Subject(s)
Antioxidants/pharmacology , Benzaldehydes/pharmacology , Bromates/adverse effects , Hair Preparations/adverse effects , Kidney/drug effects , Kidney/pathology , Adenosine Triphosphatases/metabolism , Animals , Benzothiazoles/metabolism , Biphenyl Compounds/metabolism , Environmental Pollutants/adverse effects , Kidney/metabolism , Lipid Peroxidation/drug effects , Metallothionein/genetics , Mice , Oxidative Stress/drug effects , Picrates/metabolism , Sulfonic Acids/metabolism , Up-Regulation/drug effectsABSTRACT
Chronic exposure to potassium bromate (KBrO3 ), a toxic halogen existing widely in the environment, environment through contaminated drinking water, has become a global problem of public health. The present study investigates the protective role of vanillin against KBrO3 induced oxidative stress, distruption in inflammatory cytokines expression, DNA damage, and histopathological changes. Adult mice were exposed orally to KBrO3 (2g/L of drinking water) for 2 weeks The co-administration of vanillin to the KBrO3 -treated mice significantly prevented the plasma transaminases increase in. Furthermore, it inhibited hepatic lipid peroxidation (malondialdehyde), advanced oxidation protein product (AOPP) and protein carbonyl (PCO) formation and attenuated the KBrO3 -mediated depletion of enzymatic and non enzymatic antioxidants catalase, superoxide dismutase, and glutathione peroxidase activities and glutathione level in the liver. In addition, vanillin markedly attenuated the expression levels of proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1ß, interleukin-6, and COX2 and prevented KBrO3 -induced hepatic cell alteration and necrosis, as indicated by histopathological data. DNA damage, as assessed by the alkaline comet assay, was also found to be low in the co-treated group. Thus, these findings show that vanillin acts as potent chemopreventive agent against KBrO3 -mediated liver oxidative stress and genotoxicity through its antioxidant properties. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1796-1807, 2016.
