Since the first identification of renin by Tigerstedt and Bergmann in 1898, the renin-angiotensin system (RAS) has been extensively studied. The current view of the system is characterized by an increased complexity, as evidenced by the discovery of new functional components and pathways of the RAS. In recent years, the pathophysiological implications of the system have been the main focus of attention, and inhibitors of the RAS such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin (ANG) II receptor blockers have become important clinical tools in the treatment of cardiovascular and renal diseases such as hypertension, heart failure, and diabetic nephropathy. Nevertheless, the tissue RAS also plays an important role in mediating diverse physiological functions. These focus not only on the classical actions of ANG on the cardiovascular system, namely, the maintenance of cardiovascular homeostasis, but also on other functions. Recently, the research efforts studying these noncardiovascular effects of the RAS have intensified, and a large body of data are now available to support the existence of numerous organ-based RAS exerting diverse physiological effects. ANG II has direct effects at the cellular level and can influence, for example, cell growth and differentiation, but also may play a role as a mediator of apoptosis. These universal paracrine and autocrine actions may be important in many organ systems and can mediate important physiological stimuli. Transgenic overexpression and knock-out strategies of RAS genes in animals have also shown a central functional role of the RAS in prenatal development. Taken together, these findings may become increasingly important in the study of organ physiology but also for a fresh look at the implications of these findings for organ pathophysiology.

Physiology of local renin-angiotensin systems.

Mercury is a toxic and hazardous metal that occurs naturally in the earth's crust. Natural phenomena such as erosion and volcanic eruptions, and anthropogenic activities like metal smelting and industrial production and use may lead to substantial contamination of the environment with mercury. Through consumption of mercury in food, the populations of many areas, particularly in the developing world, have been confronted with catastrophic outbreaks of mercury-induced diseases and mortality. Countries such as Japan, Iraq, Ghana, the Seychelles, and the Faroe Islands have faced such epidemics, which have unraveled the insidious and debilitating nature of mercury poisoning. Its creeping neurotoxicity is highly devastating, particularly in the central and peripheral nervous systems of children. Central nervous system defects and erethism as well as arrythmias, cardiomyopathies, and kidney damage have been associated with mercury exposure. Necrotizing bronchitis and pneumonitis arising from inhalation of mercury vapor can result in respiratory failure. Mercury is also considered a potent immunostimulant and -suppressant, depending on exposure dose and individual susceptibility, producing a number of pathologic sequelae including lymphoproliferation, hypergammaglobulinemia, and total systemic hyper- and hyporeactivities. In this review we discuss the sources of mercury and the potential for human exposure; its biogeochemical cycling in the environment; its systemic, immunotoxic, genotoxic/carcinogenic, and teratogenic health effects; and the dietary influences on its toxicity; as well as the important considerations in risk assessment and management of mercury poisoning.

Review: Environmental exposure to mercury and its toxicopathologic implications for public health

Introduction and Historical Considerations. Vitamin A. Vitamin D. Vitamin E. Vitamin K. Thiamin. Riboflavin. Niacin. Vitamin B6. Pantothenic Acid. Biotin. Folacin. Vitamin B12. Choline. Vitamin C. Vitamin-Like Substances. Essential Fatty Acids. Vitamin Supplementation. Bibliography. Appendix. Index.

Vitamin Source@@@Vitamins in Animal Nutrition: Comparative Aspects to Human Nutrition

The advent of functional imaging methods has increased our understanding of the neural control of the bladder. This review examines current concepts of the role of brain function in urinary control with particular emphasis on the putative role of dopamine receptors. Dopaminergic mechanisms play a profound role in normal bladder control and the dysfunction of these may result in symptoms of overactive bladder in Parkinsonism. The importance of this nonmotor disorder has been overlooked. We address the problem of bladder dysfunction as it presents to patients and their neurologist. The prevalence of bladder symptoms in Parkinson's disease is high; the most common complaint is nocturia followed by frequency and urgency. In multiple-system atrophy, the combination of urge and urge incontinence and poor emptying may result in a complex combination of complaints. The management of bladder dysfunction in Parkinsonism addresses treatment of overactive detrusor as well as incontinence.

Bladder dysfunction in Parkinsonism: mechanisms, prevalence, symptoms, and management.

Mercury is a ubiquitous contaminant, and a range of chemical species is generated by human activity and natural environmental change. Elemental mercury and its inorganic and organic compounds have different toxic properties, but all them are considered hazardous in human exposure. In an equimolecular exposure basis, organomercurials with a short aliphatic chain are the most harmful compounds and they may cause irreversible damage to the nervous system. Methylmercury (CH(3)Hg(+)) is the most studied following the neurotoxic outbreaks identified as Minamata disease and the Iraq poisoning. The first description of the CNS pathology dates from 1954. Since then, the clinical neurology, the neuropathology and the mechanisms of neurotoxicity of organomercurials have been widely studied. The high thiol reactivity of CH(3)Hg(+), as well as all mercury compounds, has been suggested to be the basis of their harmful biological effects. However, there is clear selectivity of CH(3)Hg(+) for specific cell types and brain structures, which is not yet fully understood. The main mechanisms involved are inhibition of protein synthesis, microtubule disruption, increase of intracellular Ca(2+) with disturbance of neurotransmitter function, oxidative stress and triggering of excitotoxicity mechanisms. The effects are more damaging during CNS development, leading to alterations of the structure and functionality of the nervous system. The major source of CH(3)Hg(+) exposure is the consumption of fish and, therefore, its intake is practically unavoidable. The present concern is on the study of the effects of low level exposure to CH(3)Hg(+) on human neurodevelopment, with a view to establishing a safe daily intake. Recommendations are 0.4 micro g/kg body weight/day by the WHO and US FDA and, recently, 0.1 micro g/kg body weight/day by the US EPA. Unfortunately, these levels are easily attained with few meals of fish per week, depending on the source of the fish and its position in the food chain.

Neurotoxicity of organomercurial compounds

/pdf/international-federation-of-associations-of-anatomists-2fs7xmxw39.pdf

International Federation of Associations of Anatomists

The existence of renin-angiotensinogen system in the rat fetal brain: I. Immunocytochemical localization of renin-like activity at the 19th day of gestation.

Angiotensinogen in the developing rat fetal hindbrain and spinal cord from 18th to 20th day of gestation: an immunocytochemical study.

The existence of renin-angiotensinogen system in the rat fetal brain: II. Immunocytochemical localization of angiotensinogen in the telencephalon and the diencephalon.

A rational pharmacological attack on heavy metal poisoning has only been possible with the advent of non-toxic binding of chelating agents. In the recent past, a number of chelators have been used to detoxicate the mercury content from the body. When all the well known chelators were subjected for their therapeutic capacities in the central nervous system, most of the findings were discouraging. In a recent study we have demonstrated the superiority of vitamins over thiol compounds in methylmercury mobilization, which otherwise has been considered difficult and often an impossible task for clinicians as well as toxicologists. Biochemical lesions are considered to be the most primary effects of methylmercury toxication, and lysosomes are the critical cellular organelles which are easily ruptured and release enzymes. In the present study, the biochemical analyses of two lysosomal enzymes (alpha and beta-galactosidases) in various nervous and non-nervous tissues of mice during methylmercury toxication as well as detoxication with vitamins and thiols have been studied in the light of previous investigation related to methylmercury mobilization with these agents. 11 refs., 2 figs.

Differential effects of methylmercury, thiols, and vitamins on galactosidases of nervous and non-nervous tissues.

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