Sadhna Srivastava

Effect of dermal application of hexachlorocyclohexane (HCH) on male reproductive system of rat

1 The toxic manifestations of dermally applied hexa chlorocyclohexane (50 mg or 100 mg kg-1 body weight day -1, 5 days in a week for 120 days) on testes and sperm of rat have been investigated. 2 The results indicate that exposure of HCH through the dermal route could lead to an alteration in the activities of marker testicular enzymes viz. sorbitol dehydrogenase (SDH), glucose-6-P-dehydrogenase (G6PDH), γ-glutamyl transpeptidase (γ-GT) and β-glucuronidase (βGluc.) associ ated with specific cell types. 3 Significant quantities of HCH and its isomers accumu lated in testes as well as sperm of treated rats. 4 HCH exposure also led to a decrease in serum testos terone levels, epididymal sperm count, sperm motility and an increase in the percentage of abnormal sperm. 5 These observations indicate the possibility of adverse effects of HCH on the male reproductive functions of men exposed dermally to this pesticide in industry or during spraying in the field.

Effect of oral administration of carbofuran on male reproductive system of rat

1 Carbofuran was administered orally to adult male rats at dose levels of 0.1, 0.2, 0.4 or 0.8 mg kg -1 body weight, 5 d wk-1 for 60 days. A dose dependent decrease was observed in body weight of rats treated with 0.2-0.8 mg carbofuran kg -1 body weight 2 A significant decrease in the weight of epididymides, seminal vesicles, ventral prostate and coagulating glands was observed at various test doses of carbofuran except at the lowest dose. 3 Decreased sperm motility, reduced epididymal sperm count along with increased morphological abnormali ties in head, neck and tail regions of spermatozoa were observed in rats exposed to 0.2, 0.4, or 0.8 mg carbo furan kg-1 body weight. 4 In addition, significant alterations were observed in the activities of marker testicular enzymes viz. sorbitol dehydrogenase (SDH), glucose-6-P-dehydrogenase (G6PDH) (decreased), lactate dehydrogenase (LDH) and γ-glutamyl transpeptidase (γ-GT) (increased) depending on dose. 5 Histologically, the results indicated the toxicity of carbo furan on testes depending on dose. The changes pre dominantly consisted of moderate oedema, congestion, damage to Sertoli cells and germ cells, along with the accumulation of cellular debris and presence of giant cells in the lumen of a few seminiferous tubules which showed disturbed spermatogenesis with the higher doses of carbofuran. 6 These observations determined a no effect level dose of 0.1 mg kg-1 body weight of carbofuran on the biochemi cal and morphological indices studied for male repro ductive toxicity assessment in the rat model. The results of the present study provide first hand information on the reproductive toxicity of carbofuran in male rats.

Effect of di(2-ethylhexyl)phthalate on 17β-hydroxysteroid dehydrogenase activity in testis of rat

The purpose of the present study was to demonstrate the effects of di(2-ethylhexyl)phthalate (DEHP) on 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity in the testis of adult rat. DEHP was administered to rats by gavage at doses of 250, 500, 1000 and 2000 mg/kg body wt./d for 15 days. The absolute and relative weights of testes were significantly decreased only at the highest dose level. The activity of 17 beta-HSD was decreased in animals exposed to 1000 and 2000 mg/kg of DEHP. The data suggest that DEHP may affect testicular steroidogenesis adversely.

Effect of styrene administration on rat testis

Styrene was administered through gavage to adult male rats for 60 days. At the lower dose of 200 mg/ kg/day no overt signs of testicular toxicity were observed, while at the higher dose of 400 mg/kg/day activities of some marker enzymes for testicular function were found to be altered significantly, along with a decrease in spermatozoa number. Histopathological studies revealed marked degeneration of seminiferous tubules and lumen devoid of sperms, further confirming testicular toxicity of styrene. The present study suggests an overall sensitivity of the male reproductive system towards styrene exposure.

Mobilization of cadmium by liposome-encapsulated meso-2,3-dimercaptosuccinic acid in pre-exposed mice.

meso-2,3-Dimercaptosuccinic acid (DMSA) treatment in free of liposome-encapsulated form was given to mice pre-exposed to cadmium as CdCl2 (2 intraperitoneal injections; 0.5 mg Cd/kg along with 5 microCi 109CdCl2 in 4 ml volume within 24 h). Both treatments removed cadmium from liver, spleen, testis and blood with liposomal DMSA exhibiting higher efficacy in mobilizing cadmium not only from whole organs but also from liver proteins. It also resulted in higher excretion of cadmium via urine as compared with free DMSA or saline treatment. Whereas this treatment eliminated significantly higher amounts of cadmium via the fecal route throughout the period examined, free DMSA responded only 48 h after treatment and was less effective. The results suggest mobilization of cadmium from intracellular sites of deposition. However, DMSA in the dose administered (24 mumol/kg i.v.) in either form was ineffective in decorporating cadmium from the kidney, the critical organ in cadmium intoxication.

Effect of liposome encapsulated meso-2,3-dimercaptosuccinic acid (DMSA) on biochemical and trace metal alterations in cadmium exposed rats

Cadmium a well known occupational and environmental contaminant, causes damage to body organs, particularly to kidneys. Considerable attention has been paid towards the development of safe and effective chelation therapy in the management of cadmium poisoning. The present communication deals with the use of liposome encapsulated DMSA, a known thiol chelator for the treatment of cadmium intoxicated rats which was found to be effective in restoring cadmium mediated biochemical and trace metal alterations.

Modulation of liposomal lipid peroxidation in presence of nickel by incorporation of a-tocopherol in the bilayer

alpha-Tocopherol is a well-known membrane associated chain-breaking phenolic antioxidant which functions as a trap for peroxyl and other free radicals and thus inhibits lipid peroxidation of membranes. Antioxidative effect of alpha-tocopherol when incorporated in liposomes was examined by the generation of Thiobarbituric acid (TBA) reacting species in the presence of nickel. The incorporation of alpha-tocopherol in the lipid bilayer resulted in the enhancement of lipid peroxidation at low concentration (1.0 mg) but at higher concentration (2.5 and 5.0 mg) considerably reduced the enhancement in lipid peroxidation of liposomes in the presence of nickel. When alpha-tocopherol was added (unincorporated) to liposomes in the presence of nickel, enhancement in lipid peroxidation was observed compared to nickel alone. Thus the antioxidative effect of alpha-tocopherol in the liposomes may depend on its mode of incorporation in the lipid bilayer.

Use of liposome encapsulated sodium‐ 2,3‐dimercapto‐propane sulfonate (DMPS) in the treatment of mice loaded with cadmium

Abstract Sodium‐2, 3‐dimercaptopropane sulfonate (DMPS) is a potent thiol chelating drug used against heavy metal intoxication. With a view to enhance its efficacy at low dose DMPS was encapsulated in liposomes made up of equimolar egg phosphotidylcholine and cholesterol and then administered to mice loaded with cadmium. Both the free as well as liposomal drug enhanced urinary excretion of cadmium. While fecal excretion of cadmium was enhanced only by liposomal drug, liposomal DMPS was effective in mobilizing more cadmium from blood, liver, kidney and spleen by day 3 of treatment, Liposomal DMPS was also able to decorporate some cadmium from cadmium binding proteins with low molecular weight corresponding to metallothionein.