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

Inorganic selenium compounds in the diet have been known to protect against cancer in laboratory animals, but were harmful in high concentrations. In the present work, the relative effects of two salts, sodium selenite and sodium selenate, administered to mice in vivo, in different concentrations and durations of exposure, were compared. Aqueous solutions of each salt (7, 14, 21 and 28 mg Kg−1 bw) were fed by gavaging to mice matched in age and sex. The animals were sacrificed at intervals of 6, 12, 18 and 24 h and chromosome preparations were made following the usual schedule of colchicine-hypotonic-fixative-airdrying-Giemsa staining. The endpoints screened were chromosomal aberrations (CA) and damaged cells (DC). Both salts affected chromosome structure and spindle formation, sodium selenite being more cytotoxic than sodium selenate. The frequencies of aberrations induced were directly proportional to the concentrations used and duration of exposure.

Comparison of clastogenic effects of inorganic selenium salts in mice in vivo as related to concentrations and duration of exposure.

Dietary consumption of green vegetables has been associated with protection against mutagenic and clastogenic activity of genotoxicants. Chlorophyll, being present in all green plants, had earlier been suggested to be the principal factor involved. Mice were administered (i) crude aqueous extract of leaf of Indian spinach, Beta vulgaris L. var.benghalensis Hort., and equivalent amounts of (ii) chlorophyll extracted from the leaf; (iii) purified chlorophyll, (iv) chlorophyllin, a sodium-copper derivative of chlorophyll; daily for 7 days. On day 7, one set of mice from each treatment was administered potassium dichromate-a known metallic clastogen. The mice were sacrificed after 24 hours. Chromosome preparations were made from bone marrow following the usual colchicine-air dry-Giemsa schedule. The cytogenetic endpoints scored were chromosomal aberrations and damaged cells. Crude leaf extract and chlorophyllin were nonclastogenic and reduced the clastogenic effects of potassium dichromate to the control distilled water level. Chlorophyll alone, whether extracted from the leaf or obtained in commercially purified form, was clastogenic and could reduce the effects of the chromium salt only to its own level. The protective action of the crude leaf extract may be attributed to the total effect of the interaction between the different components within the leaf extract, in which the clastogenicity of chlorophyll had been neutralized.

Clastogenic activity of pure chlorophyll and anticlastogenic effects of equivalent amounts of crude extract of Indian spinach leaf and chlorophyllin following dietary supplementation to mice.

Clastogenic effects of cesium chloride on mouse bone marrow cells in vivo

Frequency of sister chromatid exchanges induced by trimethyltin chloride in human peripheral blood lymphocytes as related to age of donors. A brief report.

Geeta Talukder

Papers

Comparison of clastogenic effects of inorganic selenium salts in mice in vivo as related to concentrations and duration of exposure.

Clastogenic activity of pure chlorophyll and anticlastogenic effects of equivalent amounts of crude extract of Indian spinach leaf and chlorophyllin following dietary supplementation to mice.

Clastogenic effects of cesium chloride on mouse bone marrow cells in vivo

Frequency of sister chromatid exchanges induced by trimethyltin chloride in human peripheral blood lymphocytes as related to age of donors. A brief report.

Cytotoxic effects of zirconium oxychloride on bone marrow cells of mice.