Ozone exposure induces increased production of free radicals which may result in oxidative stress. The objectives of this study were to determine the antioxidant effects of vitamin E on memory deficits and lipid peroxidation due to oxidative stress caused by acute ozone exposure. Rats were exposed to 0.7 p.p.m. ozone for 4 h and 50 mg/kg vitamin E was administered either before or after exposure. Experiment 1 evaluated alterations in short-term and long-term memory in a passive avoidance task. Experiment 2 quantified lipid peroxidation levels of the striatum, hippocampus and frontal cortex. Vitamin E administered before or after ozone exposure blocked memory deterioration and increases in lipid peroxidation levels associated with oxidative stress.
In sea urchin sperm, ionic fluxes modulate the activation of respiration and motility and the acrosome reaction, a prerequisite for egg fertilization. Ionic channels are present in the plasma membrane of these cells, and there is good evidence indicating that they are deeply involved in these processes.
The motility of spermatozoa of both Lytechinus pictus and Strongylocentrotus purpuratus sea urchin species is modulated by the egg-derived decapeptide speract via an oscillatory [Ca2+]-dependent signaling pathway. Comprehension of this pathway is hence directly related to the understanding of regulated sperm swimming. Niflumic acid (NFA), a nonsteroidal anti-inflammatory drug alters several ion channels. Though unspecific, NFA profoundly affects how sea urchin sperm respond to speract, increasing the [Ca2+]i oscillation period, amplitude, peak and average level values of the responses in immobilized and swimming cells. A previous logical network model we developed for the [Ca2+] dynamics of speract signaling cascade in sea urchin sperm allows integrated dissection of individual and multiple actions of NFA. Among the channels affected by NFA are: hyperpolarization-activated and cyclic nucleotide gated Na+ channels (HCN), [Ca2+]-dependent Cl− channels (CaCC) and [Ca2+]-dependent K+ channels (CaKC), all present in the sea urchin genome. Here, using our model we investigated the effect of blocking in silico HCN and CaCC channels suggested by experiments. Regarding CaKC channels, arguments can be provided for either their blockage or activation by NFA. Our study yielded two scenarios compliant with experimental observations: i) under CaKC inhibition, this [Ca2+]-dependent K+ channel should be different from the Slo1 channel and ii) under activation of the CaKC channel, another [Ca2+] channel not considered previously in the network is required, such as the pH-dependent CatSper channel. Additionally, our findings predict cause-effect relations resulting from a selective inhibition of those channels. Knowledge of these relations may be of consequence for a variety of electrophysiological studies and have an impact on drug related investigations. Our study contributes to a better grasp of the network dynamics and suggests further experimental work.
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