Green Tea (Camellia sinensis) Protects Against Arsenic Neurotoxicity via Antioxidative Mechanism and Activation of Superoxide Dismutase Activity

Cent Nerv Syst Agents Med Chem. 2017;17(3):187-195. doi: 10.2174/1871524917666170201145102.

Abstract

Background: Chronic arsenic-exposure even at a low-dose results in the neural impairment and motor/cognitive dysfunction. However, several preventive approaches are made mainly against hepatic/ gastrointestinal damages. Only a few investigations postulate therapeutic strategies for neural anomalies. Here, the protective role of Green tea (Camellia sinensis or CS; 10mg/ml aqueous) has been evaluated against arsenic-induced (0.6ppm/100g bw/28 days) cerebral/cerebellar tissue degeneration, oxidative-threats and neurotransmitter deregulation in female rats.

Methods and results: The Dunnett's t test and multiple-comparison ANOVA-test suggest that arsenic significantly decreased free thiol level with an increase in lipid-peroxidised product and damages to the tissue-structure. A significant decrease in serum urate accompanied by increases in C-reactive protein and TNF-α, an acute-phase inflammatory cytokine, strongly suggests a possible mechanism of oxidative- inflammatory tissue injury being supported by the increase in lactate-dehydrogenase activity. In addition, suppression in cytosolic superoxide-dismutase (Cu-Zn isoform/SOD1; NBT reduction-test) and an insufficient protection through catalase activity culminate free radical-related damages. In-vitro, H2O2 inactivated partially-purified (dialyzed/concentrated, 6-8kd cutoff-Millipore) rat liver SOD1 and that was markedly protected by 2-mercaptoethanol. Though significant signs of toxicities were noticed at biochemical/cellular level, the present treatment did not affect DNA (DNA-fragmentation assay) in the brain tissues. The CS supplementation significantly protected serum/tissue antioxidant-components, prevented inflammatory-responses and decreased lipid-peroxidation in brain resulting in increased tissue integrity. Moreover, arsenic-induced impairment of neurotransmitters i.e. glycine, glutamate and aspartate levels in cerebral tissue were significantly restored in CS-supplemented group.

Conclusion: Taken together, this investigation indicates the potent neuroprotective and antioxidative efficiencies of Camellia sinensis against arsenic-induced oxidative threat.

Keywords: Antioxidant system; DNA fragmentation; SOD1; arsenic toxicity; cytosolic; neuroprotection by Camellia sinensi.

MeSH terms

  • Animals
  • Antioxidants / isolation & purification
  • Antioxidants / pharmacology*
  • Arsenic / toxicity*
  • Brain / drug effects
  • Brain / enzymology
  • Camellia sinensis
  • Enzyme Activation / drug effects
  • Enzyme Activation / physiology
  • Female
  • Neuroprotective Agents / isolation & purification
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Plant Extracts / isolation & purification
  • Plant Extracts / pharmacology*
  • Rats
  • Superoxide Dismutase / blood*
  • Tea*

Substances

  • Antioxidants
  • Neuroprotective Agents
  • Plant Extracts
  • Tea
  • Superoxide Dismutase
  • Arsenic