Copper toxicity, oxidative stress, and antioxidant nutrients.

Turmeric, derived from the plant Curcuma longa, is a gold-colored spice commonly used in the Indian subcontinent, not only for health care but also for the preservation of food and as a yellow dye for textiles. Curcumin, which gives the yellow color to turmeric, was first isolated almost two centuries ago, and its structure as diferuloylmethane was determined in 1910. Since the time of Ayurveda (1900 Bc) numerous therapeutic activities have been assigned to turmeric for a wide variety of diseases and conditions, including those of the skin, pulmonary, and gastrointestinal systems, aches, pains, wounds, sprains, and liver disorders. Extensive research within the last half century has proven that most of these activities, once associated with turmeric, are due to curcumin. Curcumin has been shown to exhibit antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anticancer activities and thus has a potential against various malignant diseases, diabetes, allergies, arthritis, Alzheimer's disease, and other chronic illnesses. These effects are mediated through the regulation of various transcription factors, growth factors, inflammatory cytokines, protein kinases, and other enzymes. Curcumin exhibits activities similar to recently discovered tumor necrosis factor blockers (e.g., HUMIRA, REMICADE, and ENBREL), a vascular endothelial cell growth factor blocker (e.g., AVASTIN), human epidermal growth factor receptor blockers (e.g., ERBITUX, ERLOTINIB, and GEFTINIB), and a HER2 blocker (e.g., HERCEPTIN). Considering the recent scientific bandwagon that multitargeted therapy is better than monotargeted therapy for most diseases, curcumin can be considered an ideal "Spice for Life".

Curcumin: The Indian solid gold

Arsenic toxicity and potential mechanisms of action

The Analysis of Variance.

The effect of elevated temperature on mortality is a public health threat of considerable magnitude. Every year, a large number of hospitalizations and deaths occur in association with exposure to elevated ambient temperatures (1, 2). An average of 400 deaths annually are counted as directly related to heat in the United States, with the highest death rates occurring in persons aged 65 years or more (3). The actual magnitude of heat-related mortality may be notably greater than what has been reported, since we do not have widely accepted criteria for determining heat-related death (4, 5–7), and heat may not be listed on the death certificate as causing or contributing to death. Persons living in urban environments may be at particularly increased risk for mortality from ambient heat exposure, since urban areas typically have higher heat indexes (combinations of temperature and humidity (8)) than surrounding suburban or rural areas, a phenomenon known as the “urban heat island effect” (9). Moreover, urban areas retain heat during the night more efficiently (10). Thus, as the US population becomes more urbanized and the number of elderly people continues to increase (11), the threat of heat-related mortality will probably become more severe. Many of these deaths may be preventable with adequate warning and an appropriate response to heat emergencies, but preventive efforts are complicated by the short time interval that may elapse between high temperature exposure and death. Thus, prevention programs must be based around prospective and rapid identification of high-risk conditions and persons. We carried out this review to assess the current epidemiologic evidence available for this purpose.

Relation between Elevated Ambient Temperature and Mortality: A Review of the Epidemiologic Evidence

Various combinations of HgCl2 and sodium selenite were administered orally to rats and mice in vivo for both chronic and acute treatment. The antagonistic interaction and the optimum combination at which the action of HgCl2 could be neutralised by Na2SeO3 was investigated. Of the concentrations employed in rats when Na2SeO3 was fed after 1 h treatment with HgCl2, the percentage of chromosomal abnormalities significantly decreased as compared to animals treated with HgCl2 alone. All other experiments with different combinations of HgCl2 and Na2SeO3 gave higher frequencies of chromosomal abnormalities as compared to Na2SeO3 alone. An acute dose of HgCl2 was lethal, but in combination with Na2SeO3 at 1 h intervals, the abnormalities decreased to 60%. The results with mice showed antagonism in mixtures at higher doses, which was not evident in lower doses.

Effects of mercury-selenium antagonism on mammalian cell division.

Antagonistic and synergistic effects of lead and selenium in Rattus norvegicus.

Congenital malformations are a major cause of death of neonates in India where prenatal detection and treatment are not adequate in many hospitals and health centers. Incidence is specially high in stillbirths. It is not realized that genetic causes - chromosomal, single gene and polygenic - are the main causes of many congenital defects and early detection and prevention should be essential to make the small family norm a success.

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Genetic Causes of Congenital Malformation in India

The interaction between two group IV metals, the highly toxic lead and the relatively inactive and low toxic zirconium, was studied in the bone marrow chromosomes ofMus musculus in vivo. Low and high doses of zirconium oxychloride were fed orally to the experimental mice (i) 2 h before, (ii) 2 h after or (iii) together with different doses of lead nitrate. Protection against lead-induced clastogenicity was observed only when the lower dose of zirconium was administered prior to lead. All other combinations gave an additive or synergistic effect as was seen by significant increases in the frequencies of chromosomal aberrations.

Interaction between two group IV metals--lead and zirconium--in bone marrow cells of Mus musculus in vivo.

Effects of vitamin C and vitamin A were reported on the damaged bone marrow chromosomes and sister chromatid exchange studies on mice induced by both metanil yellow and zinc chioride. The results indicate that the damage is not repaired fully either naturally or by the prolonged treatment of vitamin A or vitamin C. Thus the vitamins cannot exhibit their antagonistic properties when the damage has already taken place.

Geeta Talukder

Papers

Effects of mercury-selenium antagonism on mammalian cell division.

Antagonistic and synergistic effects of lead and selenium in Rattus norvegicus.

Genetic Causes of Congenital Malformation in India

Interaction between two group IV metals--lead and zirconium--in bone marrow cells of Mus musculus in vivo.

Effects of Vitamin C and Vitamin A on Post Chromosomal Aberration in vivo Induced by Metanil Yellow and Zinc Chloride