Withania somnifera (Ashawagandha) is very revered herb of the Indian Ayurvedic system of medicine as a Rasayana (tonic). It is used for various kinds of disease processes and specially as a nervine tonic. Considering these facts many scientific studies were carried out and its adaptogenic / anti-stress activities were studied in detail. In experimental models it increases the stamina of rats during swimming endurance test and prevented adrenal gland changes of ascorbic acid and cortisol content produce by swimming stress. Pretreatment with Withania somnifera (WS) showed significance protection against stress induced gastric ulcers. WS have anti-tumor effect on Chinese Hamster Ovary (CHO) cell carcinoma. It was also found effective against urethane induced lung-adenoma in mice. In some cases of uterine fibroids, dermatosarcoma, long term treatment with WS controlled the condition. It has a Cognition Promoting Effect and was useful in children with memory deficit and in old age people loss of memory. It was also found useful in neurodegenerative diseases such as Parkinson's, Huntington's and Alzeimer's diseases. It has GABA mimetic effect and was shown to promote formation of dendrites. It has anxiolytic effect and improves energy levels and mitochondrial health. It is an anti-inflammatory and antiarthritic agent and was found useful in clinical cases of Rheumatoid and Osteoarthritis. Large scale studies are needed to prove its clinical efficacy in stress related disorders, neuronal disorders and cancers.
Berberine and Sanguinarine alkaloids belong to a group of naturally occurring chemical compounds that mostly contain basic nitrogen atoms. This group also includes some related compounds with neutral or weakly acidic properties. Alkaloids are produced by a large number of organisms including bacteria, fungi, plants, and animals. Berberine and Sanguinarine both are isoquinoline derivatives and belong to protoberberine and benzophenanthridines, respectively. Tyrosine or phenylalanine is common precursor for the biosynthesis of both. Sanguinarine [13-methyl (1,3) benzodioxolo(5,6-c)-1,3-dioxolo (4,5) phenanthridinium] is a toxin that kills animal cells through its action on the Na+-K+-ATPase transmembrane protein. Berberine, on the other hand, has been reported to cause cytotoxicity and adversely influence the synthesis of DNA. Several workers have reported varied pharmacological properties of these alkaloids as they exhibit antibacterial, antiasthma, anticancer, anti-inflammatory, and antidiabetic activities. This review article illustrates the toxicological effects of berberine and sanguinarine as well as mechanistic part of berberine and sanguinarine mediated toxicity in different living systems. This manuscript has included the lethal doses (LD50) of berberine and sanguinarine in different animals via different routs of exposure. Also, the effects of these alkaloids on the activities of some key enzymes, cell lines and organ development etc. have been summarized.
There is a widespread repeated exposure of the population to the pesticides and heavy metals of occupational and environmental origin. Such population is forced to undergo continuous stress imposed by combined exposure of the heavy metals and different classes of the pesticides used in agricultural as well as health practices. The existing reports from several workers have indicated that heavy metals and pesticides in combination may lead more severe impact on the human health when compared to their individual effects. Such a combination of pesticides and heavy metals may also change or influence the detection of exposure. Several studies in past have shown the synergistic toxic effects of heavy metals and pesticides. Such evaluations have revealed the synergistic interactions of various heavy metals and pesticides in animals as well as humans. The aim of the present article is to provide a synthesis of existing knowledge on the synergistic effects of heavy metal and pesticides in living systems. The information included in this article may be useful for different environment protection agencies and policy makers to consider the combined effects of heavy metals and pesticides on humans while designing strategies toward environmental protection and safety regulations about human health.
The effects of lead exposure on mammals are reported to be devastating. Lead is present in all the abiotic environmental components such as brass, dust, plumbing fixtures, soil, water, and lead mixed imported products. Its continuous use for several industrial and domestic purposes has caused a rise in its levels, thereby posing serious threats to human health. The mechanisms involved in lead-induced toxicity primarily include free-radical-mediated generation of oxidative stress which directly imbalances the prooxidants and the antioxidants in body. The toxicity of lead involves damage primarily to major biomolecules (lipid, protein, and nucleic acids) and liver (hepatotoxicity), nervous system (neurotoxicity), kidney (nephrotoxicity) and DNA (genotoxicity), present in animals and humans. The activation of c-Jun NH2-terminal kinase, phosphoinositide 3-kinase, or Akt and p38 mitogen activated protein kinase signaling pathways are important for lead cytotoxicity. Lead increased apoptosis through signaling cascade and associated factors and significantly impairs cell differentiation and maturation. In addition, lead has great impact on metabolic pathways such as heme synthesis, thereby leading to the onset of anemia in lead exposed people. This review encompasses an updated account of varied aspects of lead-induced oxidative stress and the biomolecular consequences such as perturbations in physiological processes, apoptosis, carcinogenesis, hormonal imbalance, loss of vision, and reduced fertility and their possible remediation through synthetic (chelators) and natural compounds (plant-based principles). This paper is primarily concerned with the biomedical implications of lead-induced generation of free radical and the toxicity management in the mammalian system.
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