Antidepressant-like effect of anacardic acid in mice via the L-arginine-nitric oxide-serotonergic system.

Depression, a multifactorial neuronal disorder with high morbidity/mortality, is associated with psychological, psychosocial, hereditary, and environmental etiologies, where reactive species exert pathophysiological functions. Anacardic acid (AA), a natural compound obtained from cashew nut liquid, has several pharmacological activities, including antioxidant and anticonvulsant. The aim of the present study was to evaluate the antidepressant-like effect of AA and the involvement of serotonergic, noradrenergic, and L-arginine-nitric oxide (NO) in tail suspension and forced swim tests and, more so, to investigate its antioxidant effect in Saccharomyces cerevisiae and in male Swiss mice (n = 8). In order to identify the antidepressant mechanisms, AA (10, 25, or 50 mg/kg, p.o.) was given 30 min before clonidine (2-adrenergic receptor agonist), L-arginine (NO precursor), propranolol (ß-adrenergic receptor antagonist), and several other agonists or antagonists used. On the other hand, clonidine, noradrenoreceptor, noradrenaline, and L-arginine were used to identify the antidepressant mechanisms. Results suggest that AA exerts antidepressant-like activity, especially at higher doses, possibly by inhibiting serotonin and 5HT-1A reuptake receptors and by inhibiting NO synthetase and guanylyl cyclase enzymes. Additionally, AA exhibited antioxidant effect in S. cerevisiae. This antioxidant capacity may be linked to its antidepressant-like effect but does not interact with α- and ß-adrenoceptor receptors. In conclusion, AA may be used as a promising agent to treat depression, especially which arises from oxidative stress.

Anxiolytic effect of anacardic acids from cashew (Anacardium occidentale) nut shell in mice.

Antianxiety drugs currently in use are associated with a number of serious side effects. Present study was designed to evaluate the efficacy of anacardic acids (AAs) isolated from cashew nut (Anacardium occidentale L.) shell liquid (CNSL) to treat anxiety as well as its role in oxidative stress in mice model. Anxiolytic effect of AA was evaluated using rota-rod and a set of behavioral tests in male Swiss albino mice at the doses of 10, 25, and 50 mg/kg. Flumazenil was used to evaluate the possible involvement of GABAergic system in the mechanism of action of AA. The effect of AA on oxidative stress in mice was evaluated by determining the concentration of malondialdehyde (MDA), reduced glutathione, and catalase (CAT) activity. The detection of DNA damage of the treated animals was performed using alkaline comet test in the hippocampus and frontal cortex of the animals. The results demonstrated that AA did not produce myorelaxant and sedative effects, nor did it cause a decrease in locomotor activity. The anxiolytic effect of AA was well-evident in all tests, especially at higher dose levels (25 and 50 mg/mg). Flumazenil reversed the anxiolytic effect of AA at all doses. In addition, AA reduced oxidative stress by decreasing the concentration of MDA and increasing the levels of reduced glutathione (GSH) and CAT activity. Statistical analysis by Pearson's correlation indicated a positive correlation between anxiolytic effect of AA to its antioxidant and lipid peroxidation inhibitory activity. Furthermore, increased CAT activity and GSH concentrations in the hippocampus and frontal cortex of mice was also complementary to the reduced genotoxic damage observed in the study. In comet assay, AA did not increase in DNA damage. In conclusion, the results supported that AA possesses GABAA receptor mediated anxiolytic activity with the lack of myorelaxation and genotoxicity. © 2018 IUBMB Life, 70(5):420-431, 2018.

Insights about levels and source appointment of petroleum hydrocarbons in Brazilian semi-arid coastal: baseline status assessment for ocean decade targets.

The Ocean decade (2021-2030) for sustainable development proclaimed in 2017 by the UN, seeks to promote and conserve the sustainable use of oceans, seas, and marine resources. For this, the distribution of n-alkanes, polycyclic aromatic hydrocarbons (PAHs), and biomarkers, in sediments from the Fortaleza coastal zone (Mucuripe harbor (MH) and Inner Continental shelf (ICS)) were used to assess the impacts of anthropogenic activities in the area. The concentrations of total n-alkanes (Σ16 n-alkanes) in MH and ICS sediments varied from 35.9 to 94.9 and 17.9 to 197.3 µg g-1, respectively, while the isoprenoids phytane and pristane in MH and ICS sediments ranged from 0.1 to 1.69 ug g-1 and from 0.14 and 1.20 µg g-1, respectively. Most of the sediment samples presented carbon preference index (CPI) values close to unity, indicating that the area is submitted to petroleum-related sources. The concentrations of Σ16 PAHs in MH and ICS sediments varied from 87.0 to 562.0 and 98 to 288.0 ng g-1. This work presents the first investigation of the petroleum biomarkers hopanes and steranes in the Fortaleza coastal zone, in which ΣBiomarkers varied from 0.10 to 1.79 and 0.02 to 0.24 ug g-1 in MH and ICS sediments, respectively. The presence at stations of biomarkers also indicates petrogenic input. The diagnosis of the distribution of pollutants in the investigated zones of the Fortaleza coast suggests contamination from urban areas and oil spills and vessel traffic.

Effects of Anacardic Acid Monoene on the Respiratory System of Mice Submitted to Acute Respiratory Distress Syndrome.

The acute respiratory distress syndrome caused by viral pathogens is a worldwide public health emergency. It is suggested that patients with this condition should be screened using therapies that address the need to prevent mortality. Anacardic acids found in Anacardium species have biological activities related to the antioxidant capacity of their double bonds in the lateral alkyl chain. The present study seeks to investigate the effects of anacardic acid monoene on acute respiratory distress syndrome caused by lipopolysaccharides. Experiments were carried out on mice divided into three groups: control group, acute respiratory distress-induced group, and anacardic acid monoene pretreated group, subsequently, induced to acute respiratory distress by lipopolysaccharides. Results showed that anacardic acid moeno was able to prevent changes in lung function and preserve its mechanical properties from containing inflammatory cell infiltrate, collapse of alveoli, and decreased airway resistance, suggesting that this compound may be effective in preventing the acute respiratory distress syndrome caused by viral pathogens. Supplementary Information: The online version contains supplementary material available at 10.1007/s43450-021-00151-8.