A convenient first aid kit for chemical and biological agents and for radiation exposure.

The chemical and biological warfare agents are extremely toxic in nature. They act rapidly even in very small quantities and death may occur in minutes. Hence, physical and medical protection must be provided immediately to save life or avoid serious injury. A first aid kit has thus been developed for providing immediate relief from chemical and biological warfare agents (FAKCBW) with the objective of easy detection, personal decontamination, antidote for chemical warfare agents (like nerve agents, sulphur mustard, phosgene, cyanide, radiation exposure and bacterial agents), along with basic medication aid for pain, fever and inflammation. The kit box also includes a user friendly handbook with a simple standard operating procedure. In addition, the kit is rugged to withstand normal jerks, vibration and is water-proof.

Dose related effects of nicotine on oxidative injury in young, adult and old rats.

Nicotine affects a variety of cellular process ranging from induction of gene expression to secretion of hormones and modulation of enzymatic activities. The objective of the present study was to study the dose dependent toxicity of nicotine on the oxidative stress in young, adult and old rats which were administered 0.75, 3 and 6 mg kg-1 nicotine as nicotine hydrogen tartarate intraperitoneally for a period of seven days. No changes were observed in blood catalase (CAT) activity and level of blood reactive oxygen species (ROS) in any of the age group at the lowest dose of nicotine. However, at the highest dose (6 mg kg-1 nicotine) ROS level increased significantly from 1.17to 1.41>M ml-1 in young rats and from 1.13 to 1.40 >M ml-1 in old rats. However, no change was observed in blood ROS levels of adult rats. Administration of 3 mg kg-1 nicotine resulted in an increase in level of reduced glutathione (GSH) in rats of all the age groups. The young animals were the most sensitive as a dose of 6 mg kg-1 resulted in decline in the levels of reduced GSH to 0.89 mg ml-1 as compared to normal control (1.03 mg ml-1). The antioxidant enzymes SOD and CAT were sensitive to a dose of 6 mg kg-1 as it resulted in decline of the enzymatic activity in all age group animals. Also, administration of nicotine at a lower dose of 3 mg kg-1 inhibited SOD activity from 1.48 to 1.20 units min-1 mg-1 protein in old rats. Catalase activity showed a similar trend at a dose of 3 mg kg-1. Administration of nicotine also increased the blood lipid peroxidation levels at all three doses in young and old rats dose dependently. Nicotine exposure also increased ROS in brain at the doses of 3 and 6 mg kg-1 in all the three age groups. Brain GSH decreased significantly at high dose of nicotine (6 mg kg-1 b.wt.) in adult rats (4.27 mg g-1) and old rats (3.68 mg g-1) but in young rats level increased to 4.40 mg g-1 at the lower dose (0.75 mg kg-1 nicotine). Brain lipid peroxidation increased at all three doses of nicotine in young as well as old rats as compared to their respective normal control. The SOD activity increased significantly in young (2.88 units min-1mg-1 protein) and old rats (1.81 units min-1mg-1 protein) as compared to their respective normal at a dose of 6 mg kg-1. Interestingly, the SOD activity decreased in adult rats (2.18 units min-1mg-1 protein) as compared to its normal control. Catalase activity decreased at the dose of 3 mg kg-1 and 6 mg kg-1 nicotine in young and old rats but no effect was observed in adult rats at any of the doses. Acetylcholine esterase (AchE) activity decreased in a dose dependent manner in adult and old rats. Overall, the results of the study indicate that young and old rats are more sensitive to nicotine induced oxidative stress as compared to the adult ones.

Arsenic and fluoride: Two major ground water pollutants.

Increasing human activities have modified the global cycle of heavy metals, non metals and metalloids. Both arsenic and fluoride are ubiquitous in the environment. Thousands of people are suffering from the toxic effects of arsenicals and fluorides in many countries all over the world. These two elements are recognized worldwide as the most serious inorganic contaminants in drinking water. Many studies have reported as regards to simple fluorosis and arsenicosis, but the knowledge of the joint action of these two elements is lacking and the results derived from previous studies were inconclusive. Contradictory results were reported in experimental studies in which different joint actions such as independent, synergistic and antagonistic effects were observed. This indicates that interaction mechanism of these two elements is considerable complicated and requires extensive studies. When two different types of toxicants are simultaneously going inside a human body they may function independently or can act as synergistic or antagonistic to one another. Thus there is an urge to resolve the question that how arsenic and fluoride act in condition of concomitant exposure. Although there have been reports in literature of individual toxicity of arsenic and fluoride however, there is very little known about the effects following the combined exposure to these toxicants. This review focused on recent developments in the research on the condition of individual exposure to arsenic and fluoride along with the recent updates of their combined exposure to better understand the joint action of these two toxicants.

Lead-induced peripheral neuropathy following ayurvedic medication.

Lead poisoning following intake of Ayurvedic medication is one of the recent areas of concern. We report a case of a 58-year-old type II diabetic man who was stable with diet control and 30 mg pioglitazone per day. He took Ayurvedic medication for generalized weakness and developed peripheral neuropathy following its intake. He was found to have high blood and urinary lead levels and was diagnosed to have subacute lead poisoning. He was treated with d-Penicillamine for 8 weeks, following which his lead levels became normal. The use of d-Penicillamine was proved highly effective in treating a case of lead poisoning.

Heavy metal induced oxidative stress & its possible reversal by chelation therapy.

Exposure to heavy metals is a common phenomenon due to their environmental pervasiveness. Metal intoxication particularly neurotoxicity, genotoxicity, or carcinogenicity is widely known. This review summarizes our current understanding about the mechanism by which metalloids or heavy metals (particularly arsenic, lead, cadmium and mercury) induce their toxic effects. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. The toxic manifestations of these metals are caused primarily due to imbalance between pro-oxidant and antioxidant homeostasis which is termed as oxidative stress. Besides these metals have high affinity for thiol groups containing enzymes and proteins, which are responsible for normal cellular defense mechanism. Long term exposure to these metals could lead to apoptosis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases and transcription factors. Chelation therapy with chelating agents like calcium disodium ethylenediamine tetra acetic acid (CaNa(2)EDTA), British Anti Lewisite (BAL), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), meso 2,3-dimercaptosuccinic acid (DMSA) etc., is considered to be the best known treatment against metal poisoning. Despite many years of research we are still far away from effective treatment against toxicity caused due to exposure to heavy metals/metalloids. The treatment with these chelating agents is compromised with number of serious side-effects. Studies show that supplementation of antioxidants along-with a chelating agent prove to be a better treatment regimen than monotherapy with chelating agents. This review attempts a comprehensive account of recent developments in the research on heavy metal poisoning particularly the role of oxidative stress/free radicals in the toxic manifestation, an update about the recent strategies for the treatment with chelating agents and a possible beneficial role of antioxidants supplementation to achieve the optimum effects. We have selected only arsenic, lead, mercury and cadmium for this article keeping in view current concerns and literature available.

Arsenic induced oxidative stress and the role of antioxidant supplementation during chelation: a review.

Arsenic is a naturally occurring metalloid, ubiquitously present in the environment in both organic and inorganic forms. Arsenic contamination of groundwater in the West Bengal basin in India is unfolding as one of the worst natural geoenvironmental disaster to date. Chronic exposure of humans to high concentration of arsenic in drinking water is associated with skin lesions, peripheral vascular disease, hypertension, Blackfoot disease and high risk of cancer The underlying mechanism of toxicity includes the interaction with the sulphydryl groups and the generation of reactive oxygen species leading to oxidative stress. Chelation therapy with chelating agents like British Anti Lewisite (BAL), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), meso 2,3 dimercaptosuccinic acid (DMSA) etc., is considered to be the best known treatment against arsenic poisoning. The treatment with these chelating agents however is compromised with certain serious drawbacks/side effects. The studies show that supplementation of antioxidants along with a chelating agent prove to be a better treatment regimen. This review attempts to provide the readers with a comprehensive account of recent developments in the research on arsenic poisoning particularly the role of oxidative stress/free radicals in the toxic manifestation, an update about the recent strategies for the treatment with chelating agents and a possible beneficial role of antioxidants supplementation to achieve the optimum effects.

Comparative hepatic and renal toxicity of cadmium in male and female rats.

Rats (male and female) were exposed to 0.5 mg/kg and 1 mg/kg cadmium as cadmium chloride for 3 days and subsequently sacrificed for cadmium concentration and other biochemical variables indicative of hepatic and renal damage. The absorption of cadmium was supported by biochemical changes, which were significantly higher in females than in males. This could be due to higher rate of intestinal absorption of cadmium in females than males. Male and female rats both showed relatively higher cadmium concentration in kidneys than in liver. Female rats also showed the similar trend in tissue metal levels as compared to male rats. However, hepatic and renal histopathological observations showed that female rats suffered from severe hepatic injury like hydropic degeneration of hepatocytes, granulation, bile duct proliferation etc. In comparison to female rats, male rats did not show much remarkable changes. Renal damage was more prominent in female than male in the form of renal tubular damage; most of the tubular nuclei were pyknotic, congestion of the boundary of cortex and medulla etc. The results suggested that females were comparatively more vulnerable to the toxic effects of cadmium than males.

Lead exposure: health effects, prevention and treatment.

This article focuses on the risk to human health associated with exposure to lead. Various human health effects associated with lead are discussed--based human and experimental data. Another important information provided in the article is regarding recent developments in the area of treatment i.e. chelation therapy against lead poisoning. Emphasis has been given to data, which have become available in the last decade.

Effects of chelation therapy on hepatic glutathione, lipid peroxidation and phospholipid contents in lead-poisoned rats.

Hepatic lipid peroxidation, glutathione and phospholipid contents of homogenate prepared from the liver of lead-intoxicated male rats treated with 0.3 m mol/kg CaNa2EDTA and DMSA for 8 weeks, either alone or in combination, were investigated. A significant increase in hepatic malondialdehyde (MDA) and a reduction in glutathione levels was noticed. While a marginal decrease in phosphatidyl choline (PC) level was noticed, no effect on phospholipid contents was seen. Treatment with all the three chelating agents elicited decrease in PC level. DMSA alone was partially effective in restoring lead-induced altered hepatic glutathione and MDA levels. Combined treatment may have an adverse effects on hepatic tissue and does not seem to produce immediate recoveries in the lead-induced hepatic damage.

Influence of selenium supplementation during chelation of lead in rats.

The influence of selenium supplementation during chelation therapy to reduce body burden and toxicity of lead was investigated in rats. Selenium had marginal effects on liver, kidney and blood lead decorporation by calcium disodium ethylenediamine tetra acetic acid (CaNa2EDTA) and activation of inhibited delta- aminolevulinic acid dehydratase (ALAD) activity by calcium trisodium diethylenetriamine penta acetic acid (CaNa3DTPA). Selenium supplementation however, had no influence on lead induced inhibition of renal and hepatic transaminases and alkaline phosphatase. The results suggest that selenium supplementation slightly augments lead mobilization by chelating drugs.

Effect of trisodium pentetat on the distribution of cadmium in some body organs & on hepatic metallothionein in rats.

The pre- and post-treatment with calcium trisodium diethylene-triaminepentaacetic acid (CaNa3DTPA) was investigated for their efficacy to mobilize cadmium (Cd) from various tissues and hepatic metallothionein (MT) in Cd-exposed rats. Pretreatment with CaNa3 DTPA significantly reduced the hepatic and renal Cd absorption while, post Cd treatment with CaNa3 DTPA was effective in reducing renal and brain Cd. Pretreatment with CaNa3DTPA significantly increased the Cd induced hepatic metallothionein (MT) level, MT-bound Cd, Zn and Cu contents while, post treatment with CaNa3DTPA reduced the hepatic MT, MT-bound Cd compared to Cd alone treated rats.

Influence oe calcium disodium edetate on the toxic effects of lead administration in pregnant rats.

Adverse effects of lead on mothers and foetal development along with lead distribution and their alteration by calcium disodium ethylenediamine tetraacetate (CaNa2EDTA) were investigated in pregnant rats. The number of fetal resorption and abnormal fetuses increased and the number of live fetuses per dam and fetal weight decreased along with increase in liver, kidney, blood, brain and fetus lead levels by lead administration. The treatment with CaNa2EDTA significantly reduced these effects of lead. However, the chelating agent enhanced the placental level of lead. Neither lead nor CaNa2EDTA altered the zinc levels of maternal organs, placenta or fetus. The results suggest that many adverse effects of lead in pregnant rats can be favourably reduced by CaNa2EDTA.