Effect of some arsenic antagonists on the toxicity, distribution and excretion of arsenite and arsenate in rats.

1. Arsenite and arsenate poisoned rats were treated with either BAL (2,3-dimercapto-1-propanol), penicillamine (PA) (beta-beta dimethyl cystein) or selenium (Se) (as sodium selenite). 2. The minimal dose of each antagonist that treated arsenic-induced lethality (causing 100% survival) was the same for both arsenite and arsenate. 3. Arsenic mobilization from the tissues (blood, kidney, liver, lungs, spleen, muscles, brain, heart) and its excretion in urine and feces were higher in arsenite-intoxicated animals than in arsenate-intoxicated ones. 4. The effect of each antagonist, when injected alone, on the urinary and fecal excretion of endogenous metals (Cu, Zn, Fe, Ca and Mg) was also examined. 5. The results indicated marked differences in the relative ability of BAL, PA and Se to increase the excretion of the metals.

Therapeutic effectiveness of 2,3,2 tet, cyclam and EDTA in toads exposed to lethal doses of nickel and cobalt.

1. In the course of the present investigation, three chelating agents (2,3,2 tet, cyclam or EDTA) were tested for their therapeutic effect on nickel and cobalt poisoned toad. 2. Our results showed that EDTA appears to be superior to the two other ligands, which have been proved to be chemical ligands for Ni and Co in vitro. 3. EDTA was able to prevent disturbances in the activities of serum aspartate and alanine aminotransferases, alkaline phosphatase, total protein, urea, uric acid and blood glucose level. 4. Our results suggest caution in the use of 2,3,2 tet or cyclam in human Ni and Co intoxication.

Acute and chronic toxicity of nitrite to Clarias lazera.

The present study is an attempt to define acute (96 hr) and chronic (6-months) effects of nitrite on two different sizes of juvenile Clarias lazera. Static bioassays on acute toxicity showed median tolerance limit (TLm) for four days of 28 and 32 mg/l NO2-N for the two sizes respectively. Although nitrite is known to cause hypoxia, as a result of oxidation of haemoglobin to methemoglobin, exposure of both sizes to nitrite resulted in a decreased erythrocyte count haemoglobin content and haematocrit values. Fish exposed to nitrite responded physiologically by producing methemoglobin. A decline in serum total protein levels was recorded during acute and chronic exposure of both sizes to nitrite. This was interpreted as a generalized stress response.

Serum transaminases activity and histopathological changes in Clarias lazera chronically exposed to nitrite.

Increase in serum transaminases (GOT and GPT) activity attributable to nitrite toxicity was observed in juvenile Clarias lazera after chronic exposure to nitrite. The application of SGOT and SGPT assays for monitoring the effect of nitrite exposure over a 6-month period has shown that changes in activities are correlated with histological effects in Clarias liver. Kidneys from fish exposed to nitrite were not noticeably different histologically from that of control fish. Hypertrophy and hyperplasia were the most consistent lesions that occurred in the gills. Lifting of lamellar epithelium and necrosis of some epithelial cells were also prominent.

Toxicity in Tilapia zilli and Clarias lazera (Pisces) induced by zinc, seasonally.

Subadult teleosts, Tilapia zilli and Clarias lazera, were exposed in laboratory bioassays to lethal and sublethal concentrations of zinc, seasonally (at range of temperature between 9.3 +/- 1.5 and 25 +/- 1 degree C). It appears that Tilapia is more susceptible to Zn than Clarias and both species are more resistant to Zn toxicity at lower temperature (during winter). To determine the uptake and tissue distribution of Zn in the two species, gill, liver and muscles were analysed at moderate temperature (during spring). After a 96 hr exposure period, Zn was decreased in the following order: gill greater than liver greater than muscle.

Some physiological and biochemical indices of zinc toxicity in two freshwater fishes, Clarias lazera and Tilapia zilli.

1. The effects of lethal zinc concentrations on some physiological and biochemical parameters in Clarias lazera and Tilapia zilli were investigated. 2. The analyses of lactate, pyruvate and glycogen in both liver and muscle tissues and the relation among them have been studied in detail. 3. Significant increases were observed in liver and serum proteins, serum alkaline phosphatase (ALP), erythrocyte count (RBCs), haematocrit or packed cell volume (PCV) and haemoglobin (HB) concentrations. 4. Zinc exposure reduced liver and serum acid phosphatase (ACP) as well as liver alkaline phosphatase (ALP).

Short-term effects of mercury on survival, behaviour, bioaccumulation and ionic pattern in the catfish (Clarias lazera).

1. The fresh-water fish, Clarias lazera, was exposed to 13 lethal and sublethal concentrations of mercury. 2. The median tolerance limit (TLm) at different exposure periods, 24, 48, 72 and 96 hr, appears to be as follows: 0.96, 0.88, 0.81 and 0.72 ppm Hg2+/l, respectively. 3. From the subacute tests, the maximum acceptable toxicant concentration (MATC) for this fish was between 0.10 and 0.22 ppm Hg2+/l. 4. Behavioural changes, tissue Hg2+ distribution and serum ionic patterns were recorded during both the acute and subacute exposure periods.

The toxicity to Clarias lazera of copper and zinc applied jointly.

1. The acute toxicity to juvenile Clarias lazera of a mixture of copper and zinc over a 96 hr exposure period was determined. Fish were exposed to the summation of half the 96 hr TLm value of each toxicant. 2. Percentage survival was much reduced indicating that the metals potentiate each others lethal action. 3. Comparison between metal residues in fish exposed to copper and zinc or to their mixture showed that the uptake of one metal was decreased by the presence of the other. 4. Toxic effects of the mixture on the physiological parameters studied were mainly attributable to copper, indicating that the presence of zinc did not influence the mode of action of copper.

Studies of Zn, Mg, Cu, Ca and Fe in cadmium poisoned toads before and after treatment with EDTA.

Zn, Mg, Cu, Ca and Fe were determined spectrophotometrically in liver, kidneys, muscle, spleen and blood of Bufo regularis after a single i.m. injection of 6.2 mg Cd/kg (which represents the 96 hr LD50) alone or in combination with 40 mg EDTA/kg (the minimal EDTA concentration causing 100% survival over that period). Cadmium administration caused recognizable effects on the essential metals levels in different tissues and organs. In the majority of the tissues and organs studied, zinc and copper concentrations returned to their normal ranges in animals that received both cadmium and EDTA. In contrast, magnesium, calcium and iron contents not only returned back to their control values but also exceeded them.

The use of the chelating agent EDTA in the treatment of acute cadmium toxicity, tissue distribution and some blood parameters in the Egyptian toad Bufo regularis.

Erythrocyte count, haemoglobin content, haematocrit value, erythrocyte sedimentation rate and cadmium accumulation in some organs and tissues were estimated in toads administered 6.2 mg Cd2+/kg i.m. for 4 days. EDTA therapy caused considerable decrease in all the blood parameters studied. A striking reduction in the cadmium content of all the organs and tissues studied except the kidneys was also observed after simultaneous treatment with EDTA.