Redox status upon herbicides application in the control of Lolium multiflorum (2n and 4n) as weed.

Lolium multiflorum Lam. is a winter weed of difficult control found as diploid (2n) and tetraploid plants (4n). Our study aimed to evaluate the responses of antioxidant enzymes and lipid peroxidation, in both diploid and tetraploid ryegrass varieties. Treatments consisted of control plants (without any herbicide application), and four herbicides with different mechanisms of action. Leaf material was collected 36 h after treatment imposition to determine the lipid peroxidation by ferrous oxidation-xylenol (FOX) content, and the activity of the enzymes superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), guaiacol peroxidase (GPX), glutathione-S-transferase (GST), and δ-aminolevulinic acid dehydratase (ALAD). Both ryegrass varieties showed oxidative stress mainly due to a downregulated decreased (>31%) in SOD activity and an increase (>32%) in lipid peroxidation (FOX), mainly in ryegrass genotypes exposed to haloxyfop, glyphosate, and iodosulfuron. On the other hand, clethodim-treated plants had an increase in SOD and APX activities, associated with a reduced ALAD activity in both 2n (32%) and 4n (11%) genotypes. In general, the 2n genotype was more affected than the 4n genotype.

α-Tocopherol regulates ectonucleotidase activities in synaptosomes from rats fed a high-fat diet.

α-Tocopherol (α-Toc) is involved in various physiologic processes, which present antioxidant and neuroprotective properties. High-fat diets have an important role in neurodegenerative diseases and neurological disturbances. This study aimed to investigate the effects of treatment with α-Toc and the consumption of high-fat diets on ectonucleotidase activities in synaptosomes of cerebral cortex, hippocampus and striatum of rats. Animals were divided into four different groups, which received standard diet (control), high-fat saturated diet (HF), α-Toc and high-fat saturated diet plus α-Toc (α-Toc + HF). High-fat saturated diet was administered ad libitum and α-Toc by gavage using a dose of 50 mg·kg(-1). After 3 months of treatment, animals were submitted to euthanasia, and cerebral cortex, hippocampus and striatum were collected for biochemical assays. Results showed that adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP) hydrolysis in the cerebral cortex, hippocampus and striatum were decreased in HF in comparison to the other groups (P < 0·05). When rats that received HF were treated with α-Toc, the activity of the ectonucleotidases was similar to the control. ATP, ADP and AMP hydrolysis in the cerebral cortex, hippocampus and striatum were increased in the α-Toc group when compared with the other groups (P < 0·05). These findings demonstrated that the HF alters the purinergic signaling in the nervous system and that the treatment with α-Toc was capable of modulating the adenine nucleotide hydrolysis in this experimental condition.

Pitaya fruit extract ameliorates the healthspan on copper-induced toxicity of Caenorhabditis elegans.

Copper (Cu) is an essential metal and it is important for metabolism. However, in high concentrations, it becomes toxic. Metal-induced toxicity is the cause of many neurodegenerative diseases. So it is necessary to search mechanisms to find ways of healthy aging. Natural compounds and diets based on fruits are increasingly common and could lead to a healthy life. Pitaya (Hylocereus undatus) is a tropical and Latin American, fruit that is gaining more popularity due to its antioxidant properties. Here, we evaluate the preventive and curative effect of different doses of microencapsulated pulp H. undatus extract on copper-induced toxicity. For this we use the nematode Caenorhabditis elegans, to investigate the effects of pitaya extract on behavior, lipid peroxidation, antioxidant chaperon, and cholinergic nervous system (ColNS). Results showed behavioral changes, decreased cell death biomarkers, and lipid peroxidation caused by copper, and these toxic effects were prevented and reverted by Pitaya's extract. After all, the extract can be used in diet as a supplement and studied to treat or prevent specific diseases, some of them linked to contamination and senility-related conditions. PRACTICAL APPLICATIONS: This research has been aimed to provide the uses of Hylocereus undatus microencapsulated pulp extract for the prevention and treatment of copper-induced toxicity. We have been shown that Pitaya is a good source of antioxidant compounds that can ameliorate the antioxidant system as well as the cholinergic nervous system avoiding behavior changes before and after the metal toxicity of copper. Therefore, the potential applications and common use of this extract can serve as food supplementation to prevent metal oxidative damage as well as to repair clinical cases of copper poisoning.

Neuroprotective and antioxidant effects of pitaya fruit on Cu-induced stress in adult zebrafish.

The harmful effects of heavy metals on organisms have not been fully described. At present, there is a close relationship between neurodegenerative diseases and copper toxicity. In addition, the copper effect on the central nervous system is followed by high levels of free radicals in different body tissues. An increase in free radical levels leads to aging-related diseases, resulting in the appearance of senile comorbidities. An increase in the consumption of natural compounds that could help to reduce this dangerous effect on organisms was observed. Pitaya (Hylocereus undatus) is a tropical fruit with great antioxidant potential and can help the organism with oxidative damage. This study evaluated the effect of H. undatus on zebrafish organisms in front of copper-induced toxicity. Therefore, the behavior, cholinergic system, antioxidant enzymes, and ALAD activity were evaluated as biomarkers. Our results highlight the great potential of Pitaya's pulp to reduce the levels of anxiety and aggressivity in fish and reduce cortisol levels. It could mediate the normal response of the cholinergic nervous system, antioxidant enzymes, and ALAD activity. Therefore, our data suggest that pitaya might improve the senile aging. PRACTICAL APPLICATIONS: The potential practical application of this study is related to the neuroprotective effect of the Hylocereus undatus microencapsulated pulp extract against metal-induced impairments. The results have shown that this extract is able to reduce the copper-induced damage modulating the antioxidant system and the cholinergic nervous system. One of the implicated potentials of use for this extract is the food supplementation to its fortification.

Fruit extract of red pitaya (Hylocereus undatus) prevents and reverses stress-induced impairments in the cholinergic and antioxidant systems of Caenorhabditis elegans.

The addition of fruit to the diet is very important, and we can use nutraceutical and functional foods for this supplement. A little-known fruit is a red pitaya (Hylocereus undatus) that has been widely reported to have a high antioxidant potential. In this study, we analyzed the in vitro and in vivo antioxidant capacity of microencapsulated pitaya extract on the behavior, antioxidant, and nervous system of the nematode Caenorhabditis elegans. The worms were treated with fruit extract before and after juglone-induced stress, to determine the protective or curative effects of pitaya. We have been evaluated cholinergic, antioxidant, and behavioral biomarkers. We have evidenced that the pulp of pitaya contains antioxidant compounds and can serve as a potential nutraceutical product. In addition, the fruit extract was effective in preventing and/or reverse the stress-induced damages, even at high levels of chemical stress at all evaluated parameters. PRACTICAL APPLICATIONS: The potential applications and uses aimed by this research are related to the supplementation of foods given the antioxidant effect. Our data suggested that the effect of the pitaya fruit microencapsulated pulp extract was effective to prevent and repair the damage caused by oxidative stress. Besides the use of this microencapsulated extract can be an auxiliary in the treatment of diseases related to oxidative damage as well as promoting senescent aging. Another important use is the application of this extract as a dietary supplement to fortify the antioxidant system.

Neuroprotective potential of Cannabis sativa-based oils in Caenorhabditis elegans.

Substances from the Cannabis sativa species, especially cannabidiol (CBD) and Delta-9-tetrahydrocannabinol (Δ9-THC), have attracted medical attention in recent years. The actions of these two main cannabinoids modulate the cholinergic nervous system (CholNS) involving development, synaptic plasticity, and response to endogenous and environmental damage, as a characteristic of many neurodegenerative diseases. The dynamics of these diseases are mediated by specific neurotransmitters, such as the GABAergic nervous system (GNS) and the CholNS. The nematode Caenorhabditis elegans is an important experimental model, which has different neurotransmitter systems that coordinate its behavior and has a transgene strain that encodes the human ß-amyloid 1-42 peptide in body wall muscle, one of the main proteins involved in Alzheimer´s disease. Therefore, the objective of this study was to evaluate the protective potential of terpenoids found in C. sativa in the GNS and CholNS of C. elegans. The effect of two C. sativa oils with variations in CBD and THC concentrations on acetylcholinesterase (AChE) activity, lipid peroxidation, and behavior of C. elegans was evaluated. C. sativa oils were efficient in increasing pharyngeal pumping rate and reducing defecation cycle, AChE activity, and ROS levels in N2 strains. In the muscle:Abeta1-42 strain, mainly when using CBD oil, worm movement, body bends, and pharyngeal pumping were increased, with a reduced AChE activity. Consequently, greater investments in scientific research are needed, in addition to breaking the taboo on the use of the C. sativa plant as an alternative for medicinal use, especially in neurodegenerative diseases, which have already shown positive initial results.

Oxidative stress and erythrocyte acetylcholinesterase (AChE) in hypertensive and ischemic patients of both acute and chronic stages.

Ischemic stroke is a leading cause of mortality and disability particularly in the elderly. Hypertension is the most important risk factor in strokes, representing roughly 70% of all cases. Oxidative stress is believed to be one of the mechanisms taking part in neuronal damage in stroke. It is well documented that cholinergic system plays a key role in normal brain functions and in memory disturbances of several pathological processes, such as in cerebral blood flow regulation. This study investigated the oxidative status and acetylcholinesterase (AChE) activity in whole blood in patients diagnosed with acute and chronic stages of ischemia, as well as with hypertension. Malondialdehyde (MDA) levels and protein carbonylation content showed increased levels both in the acute ischemic groups and in the hypertensive group, when compared to the control. Catalase activity and reduced glutathione (GSH) levels in the acute group were also higher than in the hypertensive, chronic ischemic and control groups (p<0.05). The activity of AChE in acute ischemic patients was significantly higher than that presented by the control, hypertensive and chronic ischemic patients (p<0.05). The hypertensive group presented AChE activity significantly lower than control and chronic groups. In spite of having a defined location the ischemic event results in a systemic disorder that induces changes, which can be detected by measuring the peripheral markers of oxidative stress and AChE activity in erythrocytes.

Effect of high fat diets on the NTPDase, 5'-nucleotidase and acetylcholinesterase activities in the central nervous system.

High fat diets are associated with the promotion of neurological diseases, such as Alzheimer disease (AD). This study aim investigate the high fat diets role to promotion of AD using as biochemistry parameter of status of central nervous system through the NTPDase, 5'-nucleotidase and acetylcholinesterase (AChE) activities in brain of young rats. The intake of high fat diets promotes an inhibition of purinergic and cholinergic functions, mainly in the long-term exposure to saturated and saturated/unsaturated diets. The AChE activity was decreased to supernatant and synaptosomes tissues preparations obtained from cerebral cortex in average of 20%, to both groups exposed to saturated and saturated/unsaturated diets, when compared to the control group. Very similar results were found in hippocampus and cerebellum brain areas. At same time, the adenine nucleotides hydrolysis in synaptosomes of cerebral cortex were decreased to ATP, ADP and AMP after the long-term exposure to high fat diets, as saturated and saturated/unsaturated. The inhibition of ATP hydrolysis was of 26% and 39% to saturated and saturated/unsaturated diets, respectively. ADP hydrolysis was decreased in 20% to saturated diet, and AMP hydrolysis was decreased in 25% and 33% to saturated and saturated/unsaturated diets, respectively, all in comparison to the control. Thus, we can suggest that the effects of high diets on the purinergic and cholinergic nervous system may contribute to accelerate the progressive memory loss, to decline in language and other cognitive disruptions, such as AD patients presents.

The effect of aluminium on NTPDase and 5'-nucleotidase activities from rat synaptosomes and platelets.

Aluminium (Al), a neurotoxic compound, has been investigated in a large number of studies both in vivo and in vitro. In this study, we investigated the effect in vivo of long-term exposure to Al on NTPDase (nucleoside triphosphate diphosphohydrolase) and 5'-nucleotidase activities in the synaptosomes (obtained from the cerebral cortex and hippocampus) and platelets of rats. Here, we investigated a possible role of platelets as peripheral markers in rats. Rats were loaded by gavage with AlCl(3) 50 mg/(kg day), 5 days per week, totalizing 60 administrations. The animals were divided into four groups: (1) control (C), (2) 50 mg/kg of citrate solution (Ci), (3) 50 mg/kg of Al plus citrate (Al+Ci) solution and (4) 50 mg/kg of Al (Al). ATP hydrolysis was increased in the synaptosomes from the cerebral cortex by 42.9% for Al+Ci and 39.39% for Al, when compared to their respective control (p<0.05). ADP hydrolysis was increased by 13.15% for both Al and Al+Ci, and AMP hydrolysis increased by 32.7% for Al and 27.25% for Al+Ci (p<0.05). In hippocampal synaptosomes, the hydrolysis of ATP, ADP and AMP, was increased by 58.5%, 28.5% and 25.92%, respectively, for Al (p<0.05) and 36.7%, 22.5% and 37.64% for Al+Ci, both when compared to their respective controls. ATP, ADP and AMP hydrolysis, in platelets, was increased by 172.3%, 188.52% and 92.1%, respectively in Al+Ci, and 317.9%, 342.8% and 177.9%, respectively, for Al, when compared to their respective controls (p<0.05). Together, these results indicate that Al increases NTPDase and 5'-nucleotidase activities, in synaptosomal fractions and platelets. Thus, we suggest that platelets could be sensitive peripheral markers of Al toxicity of the central nervous system.

Oxidative status in patients submitted to conization and radiation treatments for uterine cervix neoplasia.

BACKGROUND: Cervical cancer is a major cause of morbidity among women. We investigated the treatment effect on oxidative status from patients submitted to radiotherapy or conization surgery to high-grade SIL (squamous intraepithelial lesion) treatment, and oxidative profile from patients newly diagnosed for uterine cervix cancer, without treatment. METHODS: We determined the catalase activity in blood, reduced glutathione (GSH) in plasma, TBARS and protein carbonyl content from serum samples of the patients. RESULTS: The catalase activity, GSH levels, TBARS and protein carbonyl content had no statistical differences related to the controls, neither when the 2 treatments were compared, possibly because the antioxidant defense may be acting in the first period of the neoplasic transformation, and maybe indicating a possible arrest of the tumor cells caused by the efficiency of the treatments. In the non-treated patients, TBARS and protein carbonyl contents, GSH levels and catalase activity were shown to be increased comparing with the treated patients and compared with the controls indicating an tumor effect on oxidative profile, and the antioxidant activity been increased in the beginning of the tumor development. CONCLUSIONS: We suggest that the treatments were efficient in arrest of the tumor.

NTPDase and acetylcholinesterase activities in silver catfish, Rhamdia quelen (Quoy & Gaimard, 1824) (Heptapteridae) exposed to interaction of oxygen and ammonia levels

The effects of various levels of oxygen saturation and ammonia concentration on NTPDase (ecto-nucleoside triphosphate diphosphohydrolase, E.C. 3.6.1.5) and acetylcholinesterase (AChE, E.C. 3.1.1.7) activities in whole brain of teleost fish (Rhamdia quelen) were investigated. The fish were exposed to one of two different dissolved oxygen levels, including high oxygen (6.5 mg.L-1) or low oxygen (3.5 mg.L-1), and one of two different ammonia levels, including high ammonia (0.1 mg.L-1) or low ammonia (0.03 mg.L-1) levels. The four experimental groups included the following (A) control, or high dissolved oxygen plus low NH3; (B) low dissolved oxygen plus low NH3; (C) high dissolved oxygen plus high NH3; (D) low dissolved oxygen plus high NH3. We found that enzyme activities were altered after 24 h exposure in groups C and D. ATP and ADP hydrolysis in whole brain of fish was enhanced in group D after 24 h exposure by 100 percent and 119 percent, respectively, compared to the control group. After 24 h exposure, AChE activity presented an increase of 34 percent and 39 percent in groups C and D, respectively, when compared to the control group. These results are consistent with the hypothesis that low oxygen levels increase ammonia toxicity. Moreover, the hypoxic events may increase blood flow by hypoxia increasing NTPDase activity, thus producing adenosine, a potent vasodilator.(AU)

No presente estudo, avaliou-se o efeito de diferentes níveis de saturação de oxigênio e amônia sobre a atividade das enzimas NTPDase (ecto-nucleosídeo trifosfato difosfohidrolase, E.C. 3.6.1.5) e acetilcolinesterase (AChE, E.C. 3.1.1.7) em encéfalo total de jundiás (Rhamdia quelen). Os peixes foram expostos a diferentes níveis de oxigênio dissolvido e amônia, níveis altos de oxigênio (6,5 mg/L) ou baixos de oxigênio (3,5 mg/L), e níveis altos de amônia (0,1 mg/L) ou baixos de amônia (0,03 mg/L). Os peixes foram divididos em quatro diferentes grupos: (A) controle ou alto nível de oxigênio dissolvido mais baixo nível de NH3; (B) baixo nível de oxigênio dissolvido mais baixo nível de NH3; (C) alto nível de oxigênio dissolvido mais alto nível de amônia; (D) baixo nível de oxigênio dissolvido mais alto nível de NH-3. As atividades de ambas as enzimas nos grupos C e D somente foram alteradas após 24 horas de exposição. A hidrólise do ATP e ADP em encéfalo total de jundiás foi aumentada após 24h de exposição para 104 por cento e 155 por cento no grupo D quando comparado ao grupo controle, respectivamente. A atividade da AChE apresentou após 24h de exposição um aumento de 37 por cento no grupo C e 27 por cento no grupo D, ambos comparados ao grupo controle. Os resultados obtidos corroboram com a hipótese que baixos níveis de saturação de oxigênio aumentam a toxicidade da amônia. Além disso, os eventos de hipóxia podem aumentar o fluxo sanguíneo, e este evento aumenta a atividade da NTPDase produzindo adenosina, um potente vasodilatador(AU)