Exploring the neuroprotective role of melatonin against nickel-induced neurotoxicity in the left hippocampus.

Previous studies have demonstrated that the hippocampus, a crucial region for memory and cognitive functions, is particularly vulnerable to adverse effects of exposure to heavy metals. Nickel (Ni) is a neurotoxic agent that, primarily induces oxidative stress, a process known to contribute to cellular damage, which consequently affects neurological functions. The antioxidant properties of melatonin are a promising option for preventing the adverse effects of Ni, especially by protecting cells against oxidative stress and related damage. In our investigation of the potential neuroprotective effects of melatonin against Ni-induced neurotoxicity, we chose to administer melatonin through intraperitoneal injection in rats following an intrahippocampal injection of Ni into the left hippocampus. This approach allows us a targeted investigation into the influence of melatonin on the neurotoxic effects of Ni, particularly within the crucial context of the hippocampus. In the present study, we demonstrated that melatonin efficiency reduced lactate dehydrogenase level, and preserved antioxidant enzyme activities in Ni-exposed hippocampal tissue. It also mitigated the decline in superoxide dismutase and catalase activities. On the other hand, melatonin could act directly by reducing reactive oxygen species Ni-induced overproduction. Taking to gather these two potential mechanisms of action could be responsible for the adverse effect of Ni on the behavioral alteration observed in our study. This study provides significant insights into the potential of melatonin to mitigate the detrimental effects of Ni on the brain, particularly into the hippocampal region, suggesting its possible implications for the treatment of neurological disorders related to Ni exposure.

Behavioral and Amygdala Biochemical Damage Induced by Alternating Mild Stress and Ethanol Intoxication in Adolescent Rats: Reversal by Argan Oil Treatment?

Adolescence is a critical period when the effects of ethanol and stress exposure are particularly pronounced. Argan oil (AO), a natural vegetable oil known for its diverse pharmacological benefits, was investigated for its potential to mitigate addictive-like behaviors and brain damage induced by adolescent intermittent ethanol intoxication (IEI) and unpredictable mild stress (UMS). From P30 to P43, IEI rats received a daily ip ethanol (3 g/kg) on a two-day on/two-day off schedule. On alternate days, the rats were submitted to UMS protocol. Next, a two-bottle free access paradigm was performed over 10 weeks to assess intermittent 20% ethanol voluntary consumption. During the same period, the rats were gavaged daily with AO (15 mL/kg). Our results show that IEI/UMS significantly increased voluntary alcohol consumption (from 3.9 g/kg/24 h to 5.8 g/kg/24 h) and exacerbated withdrawal signs and relapse-like drinking in adulthood. Although AO treatment slightly reduced ethanol intake, it notably alleviated withdrawal signs during abstinence and relapse-like drinking in adulthood. AO's effects were associated with its modulation of the HPA axis (elevated serum corticosterone), restoration of amygdala oxidative balance, BDNF levels, and attenuation of neurodegeneration. These findings suggest that AO's neuroprotective properties could offer a potential therapeutic avenue for reducing ethanol/stress-induced brain damage and addiction. Further research is needed to explore its mechanisms and therapeutic potential in alcohol use disorders.

Melatonin modulates copper-induced anxiety-like, depression-like and memory impairments by acting on hippocampal oxidative stress in rat.

Copper (Cu) is a heavy metal with the ability to induce, at high levels, neurobehavioral alterations, and oxidative stress (OS). On the other hand, melatonin (Mel) is a neurohormone that protects neurons from OS and has a modulatory effect on several behavioral processes. The present experiment was aimed to examine the effect of Mel treatment on Cu-induced anxiety-like, depression-like behaviors, memory impairment, and OS in hippocampus. Herein, adult Wistar rats of both genders received daily Mel (4 mg/kg) thirty minutes before CuCl2 (1 mg/kg), by intraperitoneal injections for 8 weeks. After the administration period, all rats were submitted to the behavioral tests. Thereafter, OS parameters and histology of the hippocampus were evaluated. The results demonstrate that Mel treatment attenuated Cu-induced anxiety-like and depression-like behaviors, and it improved memory deficits Cu-treated rats. Furthermore, Mel attenuated Cu-provoked OS by reducing lipid peroxidation (LPO) and nitric oxide (NO) levels and enhancing superoxide dismutase (SOD) and catalase (CAT) activities in the hippocampus. The histopathological analysis also supported these results. In conclusion, these findings show that Mel treatment exerted neuroprotective effects against Cu-induced neurobehavioral changes which may be related to reduction of hippocampal OS. Besides, the effects of Cu and Mel were gender dependent, being more marked in females compared to male rats.

Anticonvulsant effect of argan oil on pilocarpine model induced status epilepticus in wistar rats.

Argan oil (AO) is rich in oleic and linoleic acids, polyphenols, sterols, and tocopherols. This composition gives it numerous beneficial pharmacological effects such as hypolipemiant, hypotensive, and antiproliferative. Oxidative stress is a mechanism of cell death induced by seizures and status epilepticus (SE). This study aims at investigating AO effects on (i) latency to first seizure, seizure severity, weight loss, mortality rate, (ii) lipid peroxidation level, nitrite level, and catalase activity in the hippocampus after SE induced by pilocarpine (PC). Wistar rats (1-month old) were daily administered by oral gavage with AO (1 ml/100 g/day) or with NaCl 0.9% during 2 months before receiving PC (400 mg/kg). After the PC injection, all groups were observed for 24 h. The catalase activity, the lipid peroxidation, and nitrite concentrations were measured using spectrophotometric methods. AO pretreatment increased the latency to first seizures, decreased the weight loss, and reduced mortality rate after SE. AO pretreatment produces significant decrease of the lipid peroxidation and nitrite levels. On the contrary, AO increased the catalase activity in rat hippocampus after seizures. For the first time, our results suggest that AO pretreatment is capable of attenuating seizure severity and oxidative stress in the hippocampus of Wistar rats. This indicates that AO may exhibit a neuroprotection against the temporal lobe epilepsy. Further investigations are in progress to confirm this pharmacological property.

Quality of life in Arab women with breast cancer: a review of the literature.

BACKGROUND: Quality of life has become an important concept in cancer care. Among the quality of lifestudies in cancer patients, breast cancer has received most attention. This review reports on quality of life in Arab patients with breast cancer. METHODS: The search was conducted using inclusion and exclusion criteria and in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The databases consulted were PubMed, Sciences Direct, Index Medicus for Wordl Health Organization Eastern Mediterranean, African Journals Online and African Index Medicus. RESULTS: Thirteen articles from eight countries met the inclusion criteria. The EORTC quality of life questionnaires (QLQ-C30 and QLQ-BR23) were the most used instrument (7 out of 13). The results showed that good scores of global health were recorded at Arab women living in United Arab Emirates (mean score = 74.6) compared to other countries. The results indicated that there was a difference in quality of life scores and its associated factors among Arab women with breast cancer. CONCLUSION: This paper is the first that reviewed published research on quality of life among Arab women with breast cancer. We found that insufficient results-related information is available.

A case report of a giant bladder stone (12 × 8 cm, 610 g).

Bladder lithiasis is common in developing countries. It has become rare in industrialized countries and exceptional in the absence of associated lower tract pathology. usually caused by urinary tract infections, urethral obstruction or the presence of intravesical foreign bodies. Open cystolithotomy was performed on a 45-year-old patient with lower abdominal pain, moderate dysuria, pollakiuria, nocturia, and hematuria for a long time. A stone of 12 × 8cm in size and approximately 620 grams in weight was removed. The cystoscopy was performed without any infravesical obstruction during the operation. The stone analysis showed 21% struvite and 79% carbonate apatite. Bladder lithiasis is common in Morocco. However, giant lithiasis is rare and is the consequence of neglected voiding disorders. Open cystolithotomy remains the most treatment in the management of giant stones.

Giant pyonephrosis related to nephrolithiasis in diabetes woman: A case report.

Pyelonephritis is one of the main systemic bacterial infections encountered in emergency departments. We present a case of diabetes woman aged 30 years referred to our urology department of El-Idrissi Hospital, Kenitra (Morocco) for recurrent episodes of urinary tract infection, multiple urolithiasis, chills, unilateral lower back pain, chills and severe hydroureteronephrosis. Abdominal CT showed a non-functioning obstructed kidney with pyelic and ureteral stones. Nephroureterectomy was performed by extraperitoneal nephrectomy for avoiding any more extended nephrectomy incision or second iliac incision, this technic ensures nephroureterectomy with minimal risk of affecting the distal ureter, that sometimes follows nephrectomy. Diabetes and urolithiasis coexistence in a patient may cause severe pyonephrosis leading to nephroureteroctomy.

Melatonin is a Neuroprotective and Antioxidant Agent against Neurotoxicity Induced by an Intrahippocampal Injection of Nickel in Rats.

The investigation into the hippocampal function and its response to heavy metal exposure is crucial for understanding the mechanisms underlying neurotoxicity, this can potentially inform strategies for mitigating the adverse effects associated with heavy metal exposure. Melatonin is an essential neuromodulator known for its efficacy as an antioxidant. In this study, we aimed to determine whether melatonin could protect against Nickel (Ni) neurotoxicity. To achieve this, we performed an intracerebral injection of Ni (300 µM NiCl2) into the right hippocampus of male Wistar rats, followed by melatonin treatment. Based on neurobehavioral and neurobiochemical assessments, our results demonstrate that melatonin efficiently enhances Ni-induced behavioral dysfunction and cognitive impairment. Specifically, melatonin treatment positively influences anxious behavior, significantly reduces immobility time in the forced swim test (FST), and improves learning and spatial memory abilities. Moreover, neurobiochemical assays revealed that melatonin treatment modulates the Ni-induced alterations in oxidative stress balance by increasing antioxidant enzyme activities, such as superoxide dismutase (SOD) and catalase (CAT). Additionally, we observed that melatonin significantly attenuated the increased levels of lipid peroxidation (LPO) and nitric oxide (NO). In conclusion, the data from this study suggests that melatonin attenuates oxidative stress, which is the primary mechanism responsible for Ni-induced neurotoxicity. Considering that the hippocampus is the main structure involved in the pathology associated with heavy metal intoxication, such as Ni, these findings underscore the potential therapeutic efficacy of melatonin in mitigating heavy metal-induced brain damage.

Melatonin attenuates affective disorders and cognitive deficits induced by perinatal exposure to a glyphosate-based herbicide via antioxidant pathway in adult male and female rats.

The massive use of herbicides, particularly glyphosate-based herbicides (GBHs), raises several worries, notably their neurotoxic effects. Several studies have explored the consequences of developmental exposure. Our work aims to determine the impact of maternal exposure to GBH on behavioral disorders and memory deficits, as well as the involvement of oxidative stress in the hippocampus and prefrontal cortex. In addition, our study explores the neuroprotective properties of melatonin in male and female offspring. Pregnant Wistar rats were injected with GBH 75 mg/kg during gestation and lactation. After weaning, the offspring were treated with melatonin (4 mg/kg) from postnatal days 30-58. Our results show that GBH increases anxiety-like behavior levels in offspring, as well as depression-like behavior. GBH also impairs working memory in progeny. While markers of oxidative stress show a disturbance in lipid peroxidation and catalase activity, with a more pronounced effect in females, on the other hand, melatonin considerably attenuated the neurotoxic impact observed in the offspring, with higher efficacy in females. The oxidative stress results confirm the antioxidant power of melatonin to counteract the damaging effects of exposure to environmental contaminants such as glyphosate-based pesticides. It will then be interesting to further our work to fully understand the sex-dependent effect of melatonin.

Evaluating the Protective Effects of Melatonin Against Chronic Iron Administration in Male Wistar Rats: a Comparative Analysis of Affective, Cognitive, and Oxidative Stress with EDTA Chelator.

Iron is the dominant metal in the brain and is distributed widely. However, it can lead to various neuropathological and neurobehavioral abnormalities as well as oxidative stress. On the other hand, melatonin, a pineal hormone, is known for its neuroprotective properties, as well as its ability to act as a natural chelator against oxidative stress. It has also been used as an antidepressant and anxiolytic. The study investigated the potential of melatonin and EDTA treatment to prevent anxiety, depressive behavior, and memory impairment in male rats induced by chronic iron administration, and its connection to oxidative stress regulation in the hippocampus and prefrontal cortex. The rats were divided into six groups and intraperitoneally injected for 8 weeks with NaCl solution (control), iron sulfate (1 mg/kg), melatonin (4 mg/kg), EDTA (4 mg/kg), 1 mg/kg of iron + 4 mg/kg of melatonin, or 1 mg/kg of iron + 4 mg/kg of EDTA. In this study, we performed a neurobehavioral assessment and biochemical determinations of oxidative stress levels in the hippocampus and prefrontal cortex of each animal. The results indicate that chronic exposure to iron sulfate induced anxiety-like depressive behavior, and cognitive impairment also increased the levels of lipid peroxidation and nitric oxide, and reduced the activity of catalase in the hippocampus and prefrontal cortex in male Wistar rats, suggesting the induction of oxidative stress. In contrast, these alterations were reversed by melatonin better than EDTA. The results of this study show that melatonin protects against the neurobehavioral changes caused by iron, which may be associated with decreasing oxidative stress in the hippocampus and prefrontal cortex.

A Systematic Review and Meta-analysis of the Association Between ACTN3 R577X Genotypes and Performance in Endurance Versus Power Athletes and Non-athletes.

BACKGROUND: Previous studies reported differences in genotype frequency of the ACTN3 R577X polymorphisms (rs1815739; RR, RX and XX) in athletes and non-athletic populations. This systematic review with meta-analysis assessed ACTN3 R577X genotype frequencies in power versus endurance athletes and non-athletes. METHODS: Five electronic databases (PubMed, Web of Science, Scopus, Science Direct, SPORTDiscus) were searched for research articles published until December 31st, 2022. Studies were included if they reported the frequency of the ACTN3 R577X genotypes in power athletes (e.g., weightlifters) and if they included a comparison with endurance athletes (e.g., long-distance runners) or non-athletic controls. A meta-analysis was then performed using either fixed or random-effects models. Pooled odds ratios (OR) were determined. Heterogeneity was detected using I2 and Cochran's Q tests. Publication bias and sensitivity analysis tests were computed. RESULTS: After screening 476 initial registrations, 25 studies were included in the final analysis (13 different countries; 14,541 participants). In power athletes, the RX genotype was predominant over the two other genotypes: RR versus RX (OR 0.70; 95% CI 0.57-0.85, p = 0.0005), RR versus XX (OR 4.26; 95% CI 3.19-5.69, p < 0.00001), RX versus XX (OR 6.58; 95% CI 5.66-7.67, p < 0.00001). The R allele was higher than the X allele (OR 2.87; 95% CI 2.35-3.50, p < 0.00001) in power athletes. Additionally, the frequency of the RR genotype was higher in power athletes than in non-athletes (OR 1.48; 95% CI 1.25-1.75, p < 0.00001). The RX genotype was similar in both groups (OR 0.84; 95% CI 0.71-1.00, p = 0.06). The XX genotype was lower in power athletes than in controls (OR 0.73; 95% CI 0.64-0.84, p < 0.00001). Furthermore, the R allele frequency was higher in power athletes than in controls (OR 1.28; 95% CI 1.19-1.38, p < 0.00001). Conversely, a higher frequency of X allele was observed in the control group compared to power athletes (OR 0.78; 95% CI 0.73-0.84, p < 0.00001). On the other hand, the frequency of the RR genotype was higher in power athletes than in endurance athletes (OR 1.27; 95% CI 1.09-1.49, p = 0.003). The frequency of the RX genotype was similar in both groups (OR 1.07; 95% CI 0.93-1.24, p = 0.36). In contrast, the frequency of the XX genotype was lower in power athletes than in endurance athletes (OR 0.63; 95% CI 0.52-0.76, p < 0.00001). In addition, the R allele was higher in power athletes than in endurance athletes (OR 1.32; 95% CI 1.11-1.57, p = 0.002). However, the X allele was higher in endurance athletes compared to power athletes (OR 0.76; 95% CI 0.64-0.90, p = 0.002). Finally, the genotypic and allelic frequency of ACTN3 genes were similar in male and female power athletes. CONCLUSIONS: The pattern of the frequencies of the ACTN3 R577X genotypes in power athletes was RX > RR > XX. However, the RR genotype and R allele were overrepresented in power athletes compared to non-athletes and endurance athletes. These data suggest that the RR genotype and R allele, which is associated with a normal expression of α-actinin-3 in fast-twitch muscle fibers, may offer some benefit in improving performance development in muscle strength and power.

Genotypic and Allelic Distribution of the CD36 rs1761667 Polymorphism in High-Level Moroccan Athletes: A Pilot Study.

Previous studies have shown that variations in the CD36 gene may affect phenotypes associated with fat metabolism as the CD36 protein facilitates the transport of fatty acids to the mitochondria for oxidation. However, no previous study has tested whether variations in the CD36 gene are associated with sports performance. We investigated the genotypic and allelic distribution of the single-nucleotide polymorphism (SNP) rs1761667 in the CD36 gene in elite Moroccan athletes (cyclists and hockey players) in comparison with healthy non-athletes of the same ethnic origin. Forty-three Moroccan elite male athletes (nineteen cyclists and twenty-four field hockey players) belonging to the national teams of their respective sports (athlete group) were compared to twenty-eight healthy, active, male university students (control group). Genotyping of the CD36 rs1761667 (G>A) SNP was performed via polymerase chain reaction (PCR) and Sanger sequencing. A chi-square (χ2) test was used to assess the Hardy-Weinberg equilibrium (HWE) and to compare allele and genotype frequencies in the "athlete" and "control" groups. The genotypic distribution of the CD36 rs1761667 polymorphism was similar in elite athletes (AA: 23.81, AG: 59.52, and GG: 16.67%) and controls (AA: 19.23, AG: 69.23, and GG: 11.54%; χ2 = 0.67, p = 0.71). However, the genotypic distribution of the CD36 rs1761667 polymorphism was different between cyclists (AA: 0.00, AG: 72.22, and GG: 27.78%) and hockey players (AA: 41.67, AG: 50.00, and GG: 8.33%; χ2 = 10.69, p = 0.004). Specifically, the frequency of the AA genotype was significantly lower in cyclists than in hockey players (p = 0.02). In terms of allele frequency, a significant difference was found between cyclists versus field hockey players (χ2 = 7.72, p = 0.005). Additionally, there was a predominance of the recessive model in cyclists over field hockey players (OR: 0.00, 95% CI: 0.00-0.35, p = 0.002). Our study shows a significant difference between cyclists and field hockey players in terms of the genotypic and allelic frequency of the SNP rs1761667 of the CD36 gene. This divergence suggests a probable association between genetic variations in the CD36 gene and the type of sport in elite Moroccan athletes.

Subchronic Exposure to Mixture of Cadmium, Copper, and Nickel Induces Neurobehavioral Deficits and Hippocampal Oxidative Stress of Wistar Rats.

The present study was aimed at evaluating the influence of the subchronic exposure of cadmium (Cd), copper (Cu), and nickel (Ni) mixtures on affective behaviors, memory impairment, and oxidative stress (OS) in the hippocampus. Thirty male Wistar rats were divided into 5 equal groups. Group 1 (control) received a saline solution (NaCl 0.9%). Groups 2, 3, and 4 received Cd (0.25 mg/kg), Cu (0.5 mg/kg), and Ni (0.25 mg/kg), respectively, while group 5 received a Cd, Cu, and Ni mixture through intraperitoneal injections for 2 months. After the exposure period, all rats were submitted to behavioral tests. Subsequently, OS markers and histological changes in the rats' hippocampi were assessed. Results showed that a 2-month exposure to the mixtures of metals (MM) has led to higher anxiety-like and depression-like behaviors and cognitive deficits in rats when compared to the control group and the individual metals. Furthermore, the MM induced heightened OS, evidenced by the rise in lipid peroxidation and nitric oxide levels. These effects were accompanied by a decrease in superoxide dismutase and catalase activities in the hippocampus. The histopathological analysis also supported that MM caused a neuronal loss in the CA3 sub-region. Overall, this study underscores that subchronic exposure to the Cd, Cu, and Ni mixture induces an OS status and histological changes in the hippocampus, with important affective and cognitive behavior variations in rats.

Potential Role of Oxidative Stress in the Effects of Chronic Administration of Iron on Affective and Cognitive Behavior on Male Wistar Rat.

In this work, we studied the impact of chronic iron exposure, in the form of iron sulfate (FeSo4), on affective and cognitive disorders and oxidative stress in the male Wistar rat. The treatment was carried out for 8 weeks, the rats received an intraperitoneal injection of iron at different doses: 0.25, 0.5, and 1 mg/kg. Affective and cognitive disorders are assessed in open field test (OFT), elevated plus maze (EPM), forced swimming test (FST), Morris water maze (MWM), and Y-maze. The hippocampus and prefrontal cortex of each animal were taken for biochemical examination. Our results show that iron exerts anxiogenic and depressogenic effects, which were observed first at the dose of 0.5 mg/kg and continued in a dose-dependent manner up to the maximum tested dose of 1 mg/kg. According to results from the MWM and Y-maze tests, continuous exposure to iron induces cognitive disorders that are defined by the disturbance of working memory and influences spatial learning performance causing a deficit of spatial memory retention. We noted that chronic exposure to iron can be associated with the appearance of a state of oxidative stress in the hippocampus and the prefrontal cortex demonstrated by an increase in lipid peroxidation, an increase in nitric oxide, and also by disturbances in the antioxidant defense systems following a determination of the concentrations of catalase. In conclusion, we can deduce from this work that chronic iron exposure can be related to the induction of cognitive and affective disorders and oxidative stress.

Association between "cluster of differentiation 36 (CD36)" and adipose tissue lipolysis during exercise training: a systematic review.

Fatty acid translocase (FAT/CD36) is a transmembrane glycoprotein belonging to the scavenger class B receptor family and is encoded by the cluster of differentiation 36 (CD36) gene. This receptor has a high affinity for fatty acids and is involved in lipid metabolism. An abundance of FAT/CD36 during exercise occurs in mitochondria and solitary muscles. As such, we aimed to systematically review the evidence for the relationship FAT/CD36 and adipose tissue lipolysis during exercise training. Five electronic databases were selected for literature searches until June 2022: PubMed, Web of Science, Scopus, science direct, and Google Scholar. We combined the different synonyms and used the operators ("AND", "OR", "NOT"): (CD36 gene) OR (CD36 polymorphism) OR (cluster of differentiation 36) OR (FAT/CD36) OR (fatty acid translocase) OR (platelet glycoprotein IV) OR (platelet glycoprotein IIIb) AND (adipose tissue lipolysis) OR (fatty acids) OR (metabolism lipid) OR (adipocytes) AND (physical effort) OR (endurance exercise) OR (high-intensity training). All published cross-sectional, cohort, case-control, and randomized clinical trials investigating CD36 polymorphisms and adipose tissue lipolysis during exercise in subjects (elite and sub-elite athletes, non-athletes, sedentary individuals and diabetics), and using valid methods to measure FAT/CD36 expression and other biomarkers, were considered for inclusion in this review. We initially identified 476 publications according to the inclusion and exclusion criteria, and included 21 studies investigating FAT/CD36 and adipose tissue lipolysis during exercise in our systematic review after examination of titles, abstracts, full texts, and quality assessments using the PEDro scale. There were nine studies with male-only participants, three with female-only participants, and nine studies included both female and male participants. There were 859 participants in the 21 selected studies. Studies were classified as either low quality (n = 3), medium quality (n = 13), and high quality (n = 5). In general, the data suggests an association between FAT/CD36 and adipose tissue lipolysis during exercise training. Improvements in FAT/CD36 were reported during or after exercise in 6 studies, while there were no changes reported in FAT/CD36 in 4 studies. An association between fat oxidation and FAT/CD36 expression during exercise was reported in 7 studies. No agreement was reached in 5 studies on FAT/CD36 content after dietary changes and physical interventions. One study reported that FAT/CD36 protein expression in muscle was higher in women than in men, another reported that training decreased FAT/CD36 protein in insulin-resistant participants, while another study reported no differences in FAT/CD36 in young, trained individuals with type 2 diabetes. Our analysis shows an association between FAT/CD36 expression and exercise. Furthermore, an association between whole-body peak fat oxidation and FAT/CD36 expression during exercise training was demonstrated. Systematic Review Registration: [PROSPERO], identifier [CRD42022342455].

Effects of Malocclusion on Maximal Aerobic Capacity and Athletic Performance in Young Sub-Elite Athletes.

Oral pathologies can cause athletic underperformance. The aim of this study was to determine the effect of malocclusion on maximal aerobic capacity in young athletes with the same anthropometric data, diet, training mode, and intensity from the same athletics training center. Sub-elite track and field athletes (middle-distance runners) with malocclusion (experimental group (EG); n = 37; 21 girls; age: 15.1 ± 1.5 years) and without malocclusion (control group (CG); n = 13; 5 girls; age: 14.7 ± 1.9 years) volunteered to participate in this study. Participants received an oral diagnosis to examine malocclusion, which was defined as an overlapping of teeth that resulted in impaired contact between the teeth of the mandible and the teeth of the upper jaw. Maximal aerobic capacity was assessed using the VAMEVAL test (calculated MAS and estimated VO2max). The test consisted of baseline values that included the following parameters: maximum aerobic speed (MAS), maximal oxygen uptake (VO2max), heart rate frequency, systolic (SAP) and diastolic arterial pressure (DAP), blood lactate concentration (LBP), and post-exercise blood lactate assessment (LAP) after the performance of the VAMEVAL test. There were no statistically significant differences between the two study groups related to either anthropometric data (age: EG = 15.1 ± 1.5 vs. CC = 14.7 ± 1.9 years (p = 0.46); BMI: EG = 19.25 ± 1.9 vs. CC = 19.42 ± 1.7 kg/m2 (p = 0.76)) or for the following physical fitness parameters and biomarkers: MAS: EG = 15.5 (14.5-16.5) vs. CG = 15.5 (15-17) km/h (p = 0.47); VO2max: EG = 54.2 (52.5-58.6) vs. CG = 54.2 (53.4-59.5) mL/kg/min (p = 0.62) (IQR (Q1-Q3)); heart rate before the physical test: EG = 77.1 ± 9.9 vs. CG = 74.3 ± 14.0 bpm (p = 0.43); SAP: EG = 106.6 ± 13.4 vs. CG = 106.2 ± 14.8 mmHg (p = 0.91); DAP: EG = 66.7 ± 9.1 vs. CG = 63.9 ± 10.2 mmHg (p = 0.36); LBP: EG = 1.5 ± 0.4 vs. CG = 1.3 ± 0.4 mmol/L (p = 0.12); and LAP: EG = 4.5 ± 2.36 vs. CG = 4.06 ± 3.04 mmol/L (p = 0.60). Our study suggests that dental malocclusion does not impede maximal aerobic capacity and the athletic performance of young track and field athletes.

Chronic clomipramine treatment reverses depressogenic-like effects of a chronic treatment with dexamethasone in rats.

Corticosteroids are widely used in medicine, for their anti-inflammatory and immunosuppressive actions, but can lead to troubling psychiatric side-effects. In fact, corticosteroids can induce many symptoms and syndromes, for example, mood disorders, anxiety and panic disorder, suicidal thinking and behavior. Furthermore, chronic stress and the administration of exogenous glucocorticoids are reported to induce affective changes in humans and rodents that relate to depressive state. Animal models are highly useful tools for studying the depression etiology. Face validity, construct validity, and predictive validity are the main criteria to evaluate animal depression models. The present study aimed to investigate the behavioral, cognitive, and biochemical effects of a chronic administration of DEX on Wistar rats. Wistar rats were administered daily with DEX (1.5 mg/kg, i.p., 21 days) or saline, the clomipramine treatment (2 mg/kg, i.p.) was realized just after the DEX injections for 21 days. DEX induced changes were evaluated by: forced swimming, novelty suppressed feeding, saccharin preference, open field, Morris water maze, and oxidative stress state in the brain. Results showed that chronic DEX administration conduct to a range of depression-related behavioral traits, including anhedonia, despair, weight loss, anxiety-like behavior, and cognitive impairments, which fill the face validity criterion. The DEX induced behavioral changes may result from the massive production of oxidative stress agents. This sustains the etiological hypothesis claiming that hyper-circulating glucocorticoid resulting from HPA dysfunction induces damage in certain neural structures related to depressive disorder, essentially the hippocampus. The antidepressant treatment has restored the behavioral state of rats which fills the predictive validity criterion.

Phosphate solubilizing rhizobacteria isolated from jujube ziziphus lotus plant stimulate wheat germination rate and seedlings growth.

Jujube plant (Ziziphus lotus (L.) Desf.) can survive in arid climates and tolerates both biotic and abiotic stresses. Here, we isolated, for the first time in Morocco, nine phosphate solubilizing bacteria strains from jujube rhizosphere, designated J10 to J13, J15, & J153 to J156. Genotypic identification based on 16S rDNA sequencing, revealed six strains that belong to Pseudomonas (J10, J12, J13, J15, J153 and J154), two to Bacillus (J11 and J156), and one to Paenibacillus J155. Siderophores were produced by all strains. Proteases activity was missing in Pseudomonas sp. J153 & J154, whereas cellulase was restricted only to Pseudomonas sp. J10, Paenibacillus xylanexedens J155 and Bacillus cereus J156. Indole-3- acetic acid and ammonia were also produced by all strains, with a maxima of 204.28 µg mL-1 in Bacillus megaterium J11 and 0.33 µmol mL-1 in Pseudomonas sp. J153, respectively. Pseudomonas sp. J10 and B. cereus J156 grew on plates containing 1,500 µg mL-1 of nickel nitrate, while Pseudomonas sp. J153 withstood 1,500 µg mL-1 of either copper sulfate or cadmium sulfate. Phenotypic analysis of the potential of the isolates to promote early plant growth showed that wheat seeds inoculated with either P. moraviensis J12 or B. cereus J156 remarkably increased germination rate and seedlings growth. Lastly, antibiotic resistance profiling revealed that except for Pseudomonas sp. J11 and B. cereus J156, remaining strains displayed resistance at least to one of tested antibiotics. Collectively, Pseudomonas sp. J10, P. moraviensis J12, Pseudomonas sp. J153 and B. cereus J156, represent potential biofertilizers suitable for soils that are poor in P, and/or heavy metals contaminated.

Melatonin Ameliorates Cadmium-Induced Affective and Cognitive Impairments and Hippocampal Oxidative Stress in Rat.

The present work aims to evaluate the effect of melatonin (Mel) on affective and cognitive disorders induced by chronic exposure to Cadmium (Cd). Male and female Wistar rats received either an intraperitoneal injection of saline solution NaCl (0.9%), Mel (4 mg/kg), Cd (1 mg/kg), or Cd (1 mg/kg) + Mel (4 mg/kg) for 8 weeks. Behavioral disorders were evaluated by different tests mainly the open field and elevated plus maze tests for anxiety-like behavior, forced swimming test (FST) for depression-like behavior, and the Y-maze and Morris water maze (MWM) tests for cognitive disorders. Thereafter, oxidative stress indices and histology of the hippocampus were evaluated. The results confirm that Cd administration has anxiogenic-like effects in both anxiety tests and depressive-like effects in the FST and leads to memory and learning disabilities in the Y-maze and MWM. We also report that Mel counteracts these neurobehavioral disorders. Biochemical assays showed that rats intoxicated with Cd significantly increased levels of nitric oxide (NO) and lipid peroxidation (LPO), while the activities of catalase (CAT) and superoxide dismutase (SOD) were significantly decreased in the hippocampus. In contrast, Mel administration attenuates the Cd-induced changes. The histopathological studies in the hippocampus of rats also supported that Mel markedly reduced the Cd-induced neuronal loss in CA3 sub-region. Overall, our results suggest that Mel could be used to protect against Cd-induced neurobehavioral changes via its antioxidant properties in the hippocampus. The effects of Cd and Mel are sex-dependent, knowing that Cd is more harmful in males, while Mel is more protective in females.

Effects of the Methyl Donors Supplementation on Hippocampal Oxidative Stress, Depression and Anxiety in Chronically High Fructose-treated Rats.

Evidence suggests that oxidative stress plays an important role in the development of anxiety and depression. The aim of the present study was to investigate whether methyl donors supplementation could exert beneficial effects on hippocampal oxidative stress, anxiety and depression in chronically high fructose-treated rats, a new animal model of anxiety and mood disorders. Rats were divided into two groups and treated for 10 weeks as follows: Group 1 represents the control group and Group 2 was treated with 23% fructose. After 10 weeks, the fructose-fed animals were divided into two groups and treated for 8 weeks as follows: Group 2 continued to receive fructose while Group 3 was treated with methyl donors and fructose. High fructose-fed rats showed increases in glucose, triglycerides, total cholesterol as well as in the final body weight and the adipose tissue weight. High fructose induced anxiety- and depression-like behaviors. High fructose caused an increase of the nitrite content and the Malondialdehyde (MDA) levels in the hippocampus tissue in association with an induction of damage in the dorsal hippocampus neurons. The 8-weeks dietary supplementation with methyl donors normalized the depression-like behavior, oxidative stress in the hippocampus, reversed the damage observed in the hippocampal neurons. These findings demonstrate that high fructose induced depression in association with the induction of a hippocampal oxidative stress. The anti-depressive action of methyl donors appears to be associated to their anti-oxidative properties since they normalized the nitrite content and the MDA levels at the hippocampus in the high fructose-fed female rats.