Protective effect of green tea against neuro-functional alterations in rats treated with MnO2 nanoparticles.

BACKGROUND: Inhalation of manganese-containing metal fumes at workplaces can cause central nervous damage including a Parkinson-like syndrome. Oxidative stress is likely to be involved in the pathomechanism, due to the presence of nano-sized metal oxide particles with high biological and chemical activity. Oxidative damage of the nervous system could be prevented or ameliorated by properly applied antioxidants, preferably natural ones such as green tea, a popular drink. The aim of this work was to see if orally applied green tea brew could diminish the functional neurotoxicity of manganese dioxide nanoparticles introduced into the airways of rats. RESULTS: Young adult male Wistar rats were treated intratracheally for 6 weeks with a suspension of synthetic MnO2 nanoparticles (4 mg/kg body weight), and received green tea brew (1 g leaves 200 mL-1 water) as drinking fluid. Reduced body weight gain, indicating general toxicity of the nanoparticles, was not influenced by green tea. However, in rats receiving green tea the nervous system effects - changes in the spontaneous and evoked cortical activity and peripheral nerve action potential - were diminished. CONCLUSION: The use of green tea as a neuroprotective functional drink seems to be a viable approach. © 2016 Society of Chemical Industry.

Green tea and vitamin C ameliorate some neuro-functional and biochemical signs of arsenic toxicity in rats.

BACKGROUND/OBJECTIVES: Nervous system damage is one of the consequences of oral exposure to waterborne inorganic arsenic. In this work, the role of oxidative status in the neurotoxicity of arsenic and the possible role of two foodborne antioxidants in ameliorating arsenic-related oxidative stress were investigated. METHODS: Male Wistar rats were given 10 mg/kg b.w. of trivalent inorganic arsenic (in the form of NaAsO2), 5 day/week for 6 weeks by gavage, combined with vitamin C solution (1 g/l) or green tea infusion (2.5 g in 500 ml boiled water) as antioxidants given in the drinking fluid. RESULTS: Body weight gain was reduced by arsenic from the second week and the antioxidants had no effect on that. Cortical evoked potentials had increased latency, tail nerve conduction velocity was reduced, and this latter effect was counteracted by the antioxidants. The effect of green tea was stronger than that of vitamin C, and green tea also diminished lipid peroxidation induced by As. There was fair correlation between brain As levels, electrophysiological changes, and lipid peroxidation, suggesting a causal relationship. DISCUSSION: Natural antioxidants might be useful in the protection of the central nervous system against the toxicity of oral As.

Rutin, a flavonoid phytochemical, ameliorates certain behavioral and electrophysiological alterations and general toxicity of oral arsenic in rats.

Arsenic affects large populations and attacks, among others, the nervous system. Waterborne or occupational exposure causes electrophysiological alterations and motor disturbances in humans, and analogous effects were found in animals. Certain phytochemicals may be protective against As-caused damages. In the present study it was investigated whether the flavonoid rutin, applied via the drinking water (2 g/L), ameliorates the effects of arsenic given by gavage (10 mg/kg b.w., in form of NaAsO2) on open field motility, evoked cortical and peripheral electrophysiological activity, and body weight gain in adult male Wistar rats. Body weight gain was significantly reduced from the 4th week of the 6 weeks arsenic treatment and this effect was largely abolished by rutin in the combination treatment group. Rats treated by arsenic alone showed decreased open field motility; latency of the cortical evoked potentials increased and peripheral nerve conduction velocity decreased. These functional alterations were also counteracted by co-administration of rutin, and both the antioxidant and the chelating activity of rutin might have contributed to the ameliorative effect. These results are apparently novel and support the potential role of natural agents in preserving human health in a contaminated environment.

Behavioral and general effects of subacute oral arsenic exposure in rats with and without fluoride.

Consequences of oral arsenic and fluoride exposure on motor behavior and general toxicity were modeled in young adult male rats which received sodium (meta)arsenite (10 mg/kg b.w.), sodium fluoride (5 mg/kg b.w.), and their combination by gavage, once daily, 5 days a week for 6 weeks. After 6 weeks, 6 animals per group were dissected, while the other 6 were kept for 6 more weeks untreated. Body weight, together with food and water consumption, was measured daily. Arsenic, alone or along with fluoride, caused significant decrease in rearing, and increase in immobility and local activity in the open field in the 3rd and 6th week. By the 12th week, these changes mostly diminished. Weight gain, and food and water consumption were significantly reduced by arsenic but normalized post treatment. Fluoride had no own effect and mostly no influence on effects of arsenic. Massive deposition of arsenic in the rats' blood, cerebral cortex, and liver by the 6th week, and partial elimination by the 12th week, was seen. The results underline the risk of neuro-functional damage by arsenic and call for further investigations.

Neuroprotection with a new kynurenic acid analog in the four-vessel occlusion model of ischemia.

Global forebrain ischemia results in damage to the pyramids in the CA1 hippocampal subfield, which is particularly vulnerable to excitotoxic processes. Morphological and functional disintegration of this area leads to a cognitive dysfunction and neuropsychiatric disorders. Treatment with N-methyl-d-aspartate receptor antagonists is a widely accepted method with which to stop the advance of excitotoxic processes and concomitant neuronal death. From a clinical aspect, competitive glycine- and polyamine-site antagonists with relatively low affinity and moderate side-effects are taken into account. Endogenous kynurenic acid acts as an antagonist on the obligatory co-agonist glycine site, and has long been at the focus of neuroprotective trials. In the present study, we estimated the neuroprotective capability of a novel kynurenic acid analog in transient global forebrain ischemia, measuring the rate of hippocampal CA1 pyramidal cell loss and the preservation of long-term potentiation at Schaffer collateral-CA1 synapses. The neuroprotective potential was reflected by a significantly diminished hippocampal CA1 cell loss and preserved long-term potentiation expression. The neuroprotective effect was robust in the event of pretreatment, and also when the drug was administered at the time of reperfusion. This result is beneficial since a putative neuroprotectant proven to be effective as post-treatment is of much greater benefit.