Moringa oleifera is an interesting plant for its use in bioactive compounds. In this manuscript, we review studies concerning the cultivation and production of moringa along with genetic diversity among different accessions and populations. Different methods of propagation, establishment and cultivation are discussed. Moringa oleifera shows diversity in many characters and extensive morphological variability, which may provide a resource for its improvement. Great genetic variability is present in the natural and cultivated accessions, but no collection of cultivated and wild accessions currently exists. A germplasm bank encompassing the genetic variability present in Moringa is needed to perform breeding programmes and develop elite varieties adapted to local conditions. Alimentary and medicinal uses of moringa are reviewed, alongside the production of biodiesel. Finally, being that the leaves are the most used part of the plant, their contents in terms of bioactive compounds and their pharmacological properties are discussed. Many studies conducted on cell lines and animals seem concordant in their support for these properties. However, there are still too few studies on humans to recommend Moringa leaves as medication in the prevention or treatment of diseases. Therefore, further studies on humans are recommended.

https://blog.baca-villa.com/wp-content/uploads/2015/10/Moringa-Oleifera-Leaves-an-Overview.pdf

Cultivation, Genetic, Ethnopharmacology, Phytochemistry and Pharmacology of Moringa oleifera Leaves: An Overview

Objective:There is burgeoning interest in augmentation strategies for improving inadequate response to antidepressants. The adjunctive use of standardized pharmaceutical-grade nutrients, known as nutraceuticals, has the potential to modulate several neurochemical pathways implicated in depression. While many studies have been conducted in this area, to date no specialized systematic review (or meta-analysis) has been conducted.Method:A systematic search of PubMed, CINAHL, Cochrane Library, and Web of Science was conducted up to December 2015 for clinical trials using adjunctive nutrients for depression. Where sufficient data were available, a random-effects model analyzed the standard mean difference between treatment and placebo in the change from baseline to endpoint, combining the effect size data. Funnel plot and heterogeneity analyses were also performed.Results:Primarily positive results were found for replicated studies testing S-adenosylmethionine (SAMe), methylfolate, omega-3 (primarily EPA or et...

https://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.2016.15091228

Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses

Moringa Oleifera (MO), a plant from the family Moringacea is a major crop in Asia and Africa. MO has been studied for its health properties, attributed to the numerous bioactive components, including vitamins, phenolic acids, flavonoids, isothiocyanates, tannins and saponins, which are present in significant amounts in various components of the plant. Moringa Oleifera leaves are the most widely studied and they have shown to be beneficial in several chronic conditions, including hypercholesterolemia, high blood pressure, diabetes, insulin resistance, non-alcoholic liver disease, cancer and overall inflammation. In this review, we present information on the beneficial results that have been reported on the prevention and alleviation of these chronic conditions in various animal models and in cell studies. The existing limited information on human studies and Moringa Oleifera leaves is also presented. Overall, it has been well documented that Moringa Oleifera leaves are a good strategic for various conditions associated with heart disease, diabetes, cancer and fatty liver.

Bioactive Components in Moringa Oleifera Leaves Protect against Chronic Disease

Lead toxicity is a major public health issue in developed and developing countries. Both acute and chronic lead exposure has the potential to cause many deleterious systematic effects including hypertension, frank anemia, cognitive deficits, infertility, immune imbalances, delayed skeletal and deciduous dental development, vitamin D deficiency, and gastrointestinal effects. The underlying mechanisms for all these systemic effects have not been elucidated completely. However, the most plausible cause is free radical damage. In addition to this, lead being a divalent cation can surrogate for calcium at multiple levels affecting various cell signaling pathways. The molecular basis of lead exposure resulting in various systemic effects is being extensively explored. The reports include single nucleotide polymorphisms, epigenetic modifications in susceptible individuals, and the most recent reports also feature regulatory RNA molecules - miRNAs. However, many genetic targets are identified, but their possible mechanisms are still an area to be explored. Additional studies are needed in different population groups to validate the existing findings, as well as to find newer targets that may help in better understanding the molecular mechanisms contributing to lead toxicity. Furthermore, newer strategies for lead risk assessment becomes necessary as the previously recognized "safe" level of lead is also being found to be associated with negative health outcomes.

Clinical and molecular aspects of lead toxicity: An update

Oxidative stress is generally considered as the consequence of an imbalance between pro- and antioxidants species, which often results into indiscriminate and global damage at the organismal level. Elderly people are more susceptible to oxidative stress and this depends, almost in part, from a decreased performance of their endogenous antioxidant system. As many studies reported an inverse correlation between systemic levels of antioxidants and several diseases, primarily cardiovascular diseases, but also diabetes and neurological disorders, antioxidant supplementation has been foreseen as an effective preventive and therapeutic intervention for aging-associated pathologies. However, the expectations of this therapeutic approach have often been partially disappointed by clinical trials. The interplay of both endogenous and exogenous antioxidants with the systemic redox system is very complex and represents an issue that is still under debate. In this review a selection of recent clinical studies concerning antioxidants supplementation and the evaluation of their influence in aging-related diseases is analyzed. The controversial outcomes of antioxidants supplementation therapies, which might partially depend from an underestimation of the patient specific metabolic demand and genetic background, are presented.

/pdf/antioxidant-supplementation-in-the-treatment-of-aging-2re6ago17x.pdf

Antioxidant Supplementation in the Treatment of Aging-Associated Diseases

The recognition of vitamin C is associated with a history of an unrelenting search for the cause of the ancient haemorrhagic disease scurvy. Isolated in 1928, vitamin C is essential for the development and maintenance of connective tissues. It plays an important role in bone formation, wound healing and the maintenance of healthy gums. Vitamin C plays an important role in a number of metabolic functions including the activation of the B vitamin, folic acid, the conversion of cholesterol to bile acids and the conversion of the amino acid, tryptophan, to the neurotransmitter, serotonin. It is an antioxidant that protects body from free radical damage. It is used as therapeutic agent in many diseases and disorders. Vitamin C protects the immune system, reduces the severity of allergic reactions and helps to fight off infections. However the significance and beneficial effect of vitamin C in respect to human disease such as cancer, atherosclerosis, diabetes, neurodegenerative disease and metal toxicity however remains equivocal. Thus further continuous uninterrupted efforts may open new vistas to understand its significance in disease management.

/pdf/vitamin-c-in-disease-prevention-and-cure-an-overview-aeya39os1l.pdf

Vitamin C in Disease Prevention and Cure: An Overview

The lead exposure is a public health concern, especially in early childhood as children are more at risk because of increased hand to mouth activity and absorb about half of an oral dose of water-soluble lead [1]. Childhood lead exposure is estimated to contribute to 600,000 new cases of children with intellectual disabilities every year with 99 % of them living in developing countries [2]. The lead exposure in utero, infancy or early childhood can slow mental development and cause lower intelligence later in childhood that can persist beyond childhood. The effects of lead are more toxic on developing nervous system of children than on a mature brain.

Lead-associated deficits have been documented in most fields including verbal intelligence quotient (IQ), performance IQ, academic skills such as reading and mathematics, visual/spatial skills, problem-solving skills, executive functions, fine and gross motor skills, memory and language skills. Meta-analyses have indicated that children’s IQ scores decline 2–3 points per 10 ug/dl increase in blood lead level [3] and identified no threshold for the effects of lead on IQ [4]. In fact academic performance of children exposed to lead has been observed to be subservient in comparison to controls. Children (6–10 year old) with blood lead levels of 5–10 ug/dl scored significantly lower than children with levels of 1–2 ug/dl on academic skills such as word reading, reading comprehension, listening comprehension, math reasoning and math calculations [3]. Another large American study documented inverse association between blood lead levels as low as 2 ug/dl, measured up to 5 years of age, and end-of-grade reading and mathematics achievement scores [5]. In National Health and Nutrition Examination Survey (1999–2002), the risk of parent-reported diagnosis of attention deficit hyperactivity disorder increased, in a dose-dependent manner with blood lead level [3]. Similar findings have been reported by a recent Indian study which emphasizes the detrimental effect of lead on executive and attention domain in neurobehavioral function [6].

The mechanisms underlying lead-induced neurotoxicity are complex. Oxidative stress, membrane bio-physics alterations, deregulation of cell signaling, and the impairment of neurotransmission are key aspects involved in lead neurotoxicity. It can cause toxicity by oxidative stress directly or indirectly by lipid peroxidation resulting in the generation of reactive oxygen species (ROS), including hydroperoxides, singlet oxygen, hydrogen peroxide and direct depletion of antioxidant reserves. Lead renders enzymes nonfunctional by binding to their sulfhydryl groups further contributing to an impairment in oxidative balance [7].

The ability of lead to pass through the blood–brain barrier is mainly due to its ability to substitute for calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve damage, and possibly Alzheimer’s disease, Parkinson’s disease and schizophrenia [8]. Lead substitutes for calcium and to a lesser extent zinc, inappropriately triggers processes dependent on calmodulin. Lead also restricts neurotransmitter release, disrupting the function of GABAergic, dopaminergic and cholinergic systems as well as inhibiting NMDA-ion channels during the neonatal period. Indeed experimental studies have shown that lead activates protein kinase C in capillary cells and inhibits Na+/K+-ATPase thus interfering with energy metabolism. Within the cell, lead appears to interfere with calcium release from the mitochondria resulting in formation of permeability transition pore and primes for programmed cell death processes leading to mitochondrial self-destruction [9]. Hence direct neurotoxic actions of lead include apoptosis, excitotoxicity affecting neurotransmitter storage, release and modifying neurotransmitter receptors, mitochondria, second messengers, cerebrovascular endothelial cells, astroglia and oligodendroglia.

Mechanisms underlying cognitive deficits resultant of lead exposure have been reported using cellular models of learning and memory. There is convincing evidence that exposures to lead have adverse effects on the central nervous system (CNS), environmental factors augment lead susceptibility and exposures in early life can cause neurodegeneration in later life. Magnetic resonance spectroscopy (MRS) has revealed reductions in the N-acetylaspartate-to-creatine and phosphocreatine ratios in the frontal gray matter of lead-exposed children, consistent with increased neuronal loss. Similarly in adults an association between greater cumulative lead exposure and higher myoinositol-to-creatine ratios in the hippo-campus, reflecting glial dysfunction has been seen [3].

With the development of molecular biology, the knowledge of genetics has been incorporated into the environmental health research. The individual genetic profile has to be taken into account in investigating the toxic effect of lead. Likewise, the gene encoding δ-amino levulinic acid dehydratase (ALAD), an enzyme actively involved in leadership kinetics, could make a portion of the population with some ALAD genotype more susceptible to lead toxicity [10]. As such, these people need special attention and protection. It is of public health importance to figure out which allele is the susceptible one and how it operates in the human body. The human data available on chelation efficacy suggest that primary prevention of exposure is the best strategy for limiting lead-associated neurodevelopmental morbidity [9].

/pdf/lead-and-neurotoxicity-25s3uotvue.pdf

Lead and Neurotoxicity

The aim of this review was to provide current scenario linking obesity and male fertility. Obesity has been linked to male fertility because of lifestyle changes, internal hormonal environment alterations, and sperm genetic factors. A few studies assessing the impact of obesity on sperm genetic factor have been published, but they did not lead to a strong consensus. Our objective was to explore further the relationship between sperm genetic factor and obesity. There are emerging facts that obesity negatively affects male reproductive potential not only by reducing sperm quality, but in particular it alters the physical and molecular structure of germ cells in the testes and ultimately affects the maturity and function of sperm cells. Inhibition of microRNA in the male pronucleus of fertilized zygotes produces offspring of phenotypes of variable severity depending on miRNAs ratios. Hence, these RNAs have a role in the oocyte development during fertilization and in embryo development, fetal survival, and offspring phenotype. It has been reported that the miRNA profile is altered in spermatozoa of obese males, however, the impact of these changes in fertilization and embryo health remains as yet not known.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/andr.270

Recent scenario of obesity and male fertility.

Lead ranks as one of the most serious environmental poisons all over the world amongst toxic heavy metals with no known biological function useful for the human body. A case of lead toxicity due to consumption of herbal medicine is being discussed. The case presented with gastrointestinal complaints and history of intake of herbal medicines for diabetes control for past 8 months. The analysis of the powdered herbal medicine procured from ayurveda practitioner was found to have high content of lead responsible for the lead toxicity. The patient is under regular followup. He has improved symptomatically on chelating therapy and blood lead levels have gradually improved. Regular awareness programs should be conducted in the population regarding possible exposure through home made herbal remedies so that general public can be made aware of the dangerous side effects of lead and other heavy metals on health.

Lead Poisoning Due to Herbal Medications.

Lead interferes with a variety of body processes and is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. Routes of exposure to lead include contaminated air, water, soil, food, and consumer products. The possibility of lead exposure in humans is therefore of great significance from health point of view. Occupational exposure is a common known cause of lead poisoning in adults but current status of adults exposed otherwise is not known. School teachers representing wide local population were selected and asked to furnish information regarding possible lead exposure. Blood lead level (BLL) was estimated using anodic stripping voltammetry. The mean BLL was 6.89 ± 9.5 μg/dl ( 65 μg/dl) in representative adult population. Out of the total 16 % were found to be having BLL >10 μg/dl which has significantly decreased from leaded gasoline era. Those with increased BLL (>10 μg/dl) were found to have common determinants like usage of old metallic pipes for plumbing, water consumption without any purification system, usage of cosmetics and Ayurvedic/herbal medicines.

Shailja Chambial

Papers

Vitamin C in Disease Prevention and Cure: An Overview

Lead and Neurotoxicity

Recent scenario of obesity and male fertility.

Lead Poisoning Due to Herbal Medications.

Blood Lead Level (BLL) in the Adult Population of Jodhpur: A Pilot Study