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Biomedical subjects

D K Saxena

Publications and source records attributed to D K Saxena.

At least 55 records · Page 3Linked to original sources
PubMed1995

Chromium fetotoxicity in mice during late pregnancy.

Female mice received 250, 500 or 750 ppm chromium (VI) as potassium dichromate in drinking water on days 14 to 19 of pregnancy. Gestational weight gain of mothers, fetal weight and crown-rump length decreased in the 500 and 750 ppm groups. The high-dose group also had significantly higher incidences of postimplantation loss. Significant increases in drooping wrists, subdermal hemorrhagic patches, kinky and short tails, and reduced ossification were also found in the 750 ppm group. Chromium levels were increased in a dose-dependent manner in maternal blood and placenta and in fetuses. Our study suggests a risk to the developing fetus if the mother is exposed to high concentrations of chromium (VI) during pregnancy.

Administration, Oral↗
PubMed1995

Endosulfan-induced biochemical changes in the testis of rats.

Adult male rats were exposed to 0, 2.5, 5.0 or 10.0 mg endosulfan/kg body weight through oral intubation for 70 d. Decreased sperm counts in the cauda epididymis and reduced intratesticular spermatid counts associated with elevation in the activities of specific testicular marker enzymes (sorbitol dehydrogenase, lactic dehydrogenase, gamma glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase) were seen in all the endosulfan-dosed groups. Endosulfan caused impairment in testicular functions by altering activities of the enzymes responsible for spermatogenesis, thereby influencing intratesticular spermatid count and causing low sperm production and sperm deformity.

Administration, Oral↗
PubMed1993

Embryo-fetal development influenced by lead exposure in iron-deficient rats.

Lead administered (250, 500, 1000 and 2000 ppm Pb as lead nitrate) through drinking water from the 6th to the 14th day of gestation in iron-deficient rats, resulted in a significantly reduced litter size, reduced fetal weight and a reduced crown-rump length, increased resorption and a higher blood-lead uptake in those groups receiving 1000 and 2000 ppm Pb. These animals also had a higher placental lead uptake. However, the level was the same in both groups. Fetal lead uptake remained the same whether or not 2000 ppm lead was given to an iron-deficient or normal iron groups of mothers. This indicates that iron-deficiency renders female rats more susceptible to inducing embryo- and feto-toxicity when given lead through their drinking water.

Animals↗
PubMed1993

Right thoracotomy revisited.

From September 1991 through August 1992, 38 patients (34 female and 4 male) underwent mitral valve surgery through a limited right anterior thoracotomy. The ascending aorta was easily cannulated for arterial return in all patients. Although there was no operative mortality, 8 patients required reoperation for bleeding, usually associated with the site of chest-wall puncture for the left atrial pressure line and epicardial pacing wires, a problem that we were able to correct. Right lower lobe collapse occurred in 2 patients, but the lungs were fully expanded in all patients before hospital discharge. We believe that a return to this older surgical approach is particularly suited to young patients and provides the important advantages over median sternotomy of superior mitral valve exposure and a cosmetically acceptable scar.

Adolescent↗
PubMed1991

Ultrastructural observations in testicular tissue of chromium-treated rats.

The administration of hexavalent chromium (2 mg/kg, ip as potassium dichromate) in adult rats daily for 15 days produced significant increases in the blood and testicular chromium levels. Although no light microscopic pathologic changes or alterations in epididymal sperm counts and motility were observed, lanthanum perfusion in treated rats revealed leakage of Sertoli-cell tight junctions under EM. A few tubules showed marked ultracellular alterations in the form of vacuolization of cytoplasm and degeneration of mitochondria in the epithelial cells. Late stage spermatids were the most affected germ cells. The mitochondrial sheath of the midpiece was vacuolated, incomplete, swollen, or broken in places. The observed alterations may result in the disruption of normal testicular physiology leading to reproductive impairment after chromium exposure.

Animals↗
PubMed1991

Lead-induced fetal nephrotoxicity in iron-deficient rats.

Lead administration (250, 500, 1000, and 2000 ppm, as lead acetate) in drinking water during fetal development (from 15 to 20 days of gestation), in normal and iron-deficient pregnant rats, revealed dose-dependent increases in the lead content of maternal blood that was more marked in iron-deficient animals. The placentae and fetuses did not show a dose-dependent increase in lead content. Lead administration revealed dose-dependent hydropic degeneration of renal proximal cells in the fetuses. The highest dose (2000 ppm lead) and iron deficiency exhibited more lead accumulation in maternal blood, placentae, and fetuses, and maximum pathologic changes in the fetal kidney when compared with the other doses and also with the fetuses of dams not deficient in iron.

Animals↗
PubMed1991

Lead induced ultrastructural changes in the testis of rats.

Oral lead administration (250 ppm lead acetate through drinking water) to weaning male rats for 70 days resulted in the marked accumulation of this metal in blood and testicular tissue. No marked changes were evident in light microscopy. Ultrastructural changes were revealed in the form of vacuolisation of Sertoli cell cytoplasm and increase in the number and size of lysosomes. Some of the vacuoles contained vesicle like structures. Although there was no impairment of spermatogenesis, the changes in the Sertoli cells may lead to changes in spermatogenesis after chronic exposure.

Administration, Oral↗
PubMed1990

Testicular effects of di-n-butyl phthalate (DBP): biochemical and histopathological alterations.

Di-n-butyl phthalate (DBP) was administered to young male rats by gavage at the doses of 250, 500 and 1,000 mg/kg body weight/day for 15 days. A significant decrease in testes weight was observed at 500 and 1,000 mg/kg doses of DBP. Histopathological examination revealed marked degeneration of seminiferous tubules. The activities of testicular enzymes associated with postmeiotic spermatogenic cells, such as sorbitol dehydrogenase and acid phosphatase, were decreased significantly, while that of lactate dehydrogenase was significantly increased, coincident with degeneration of spermatogenic cells. The activities of enzymes associated with premeiotic spermatogenic cells, Sertoli cells or interstitial cells, beta-glucuronidase, gamma-glutamyl transpeptidase and glucose-6-phosphate dehydrogenase were significantly increased. Thus the alterations in activity of these testicular cell specific enzymes suggest that DBP exposure during early life could affect the testicular functions.

Animals↗
PubMed1990

Effect of hexavalent chromium on testicular maturation in the rat.

Daily intraperitoneal administration of hexavalent chromium (Cr6+; 1, 2, and 3 mg/kg intraperitoneally as potassium dichromate) in weaned rats for an entire duration of 55 and 90 days of age produced dose- and duration-dependent enzymatic and pathologic alterations. At 55 days, the pathologic changes were not seen in testes of Cr6+ treated rats, but the activities of sorbitol dehydrogenase, lactic dehydrogenase, gamma-glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase were significantly altered. When the treatment was prolonged to sexual maturity, that is, 90 days of age, the alterations in enzyme activities were greater, and there were dose-dependent pathologic changes in the testes of Cr(6+)-treated rats. These alterations suggest a risk to growing testes if rats are exposed to Cr6+ during the prepubertal stage of development, which, in turn, may disturb normal testicular physiology at adulthood.

Animals↗
PubMed1990

Lead induced testicular hypersensitivity in stressed rats.

Rats were immobilized for 2 h and treated i.p. with lead Pb2+ (8 mg/kg/day) for 45 d to investigate the testicular effects of lead on rats kept under immobilization stress. Marked alteration in SDH. G6PDH activity, cholesterol and ascorbic acid contents and reduced sperm counts associated with marked pathological changes in the testis of rats were observed after combined treatment with lead and immobilization stress in comparison to either alone. An increase in the disturbances of testicular androgen synthesis seems to be responsible for enhanced testicular injury in lead induced stressed rats.

Animals↗
PubMed1989

Embryotoxicity and fetotoxicity of orally administered hexavalent chromium in mice.

The embryotoxic and fetotoxic potential of hexavalent chromium (Cr+6) in mice was investigated by administering 250, 500, and 1000 ppm of potassium dichromate daily through drinking water during the entire gestation period. An increase in embryonic deaths was observed; however, in the mothers treated with the highest dose, there was complete absence of implantation sites. No major abnormality was observed in the fetuses except that Cr+6 exposure increased the incidences and types of external and skeletal malformations. It is concluded that oral exposure to Cr+6 causes dose-dependent embryolethal effects in mice.

Abnormalities, Drug-Induced↗
PubMed1989

Lead induced testicular changes in protein malnourished rats.

The effect of concurrent low protein (8% casein) diet and lead (Pb) exposure (1 mg/ml lead acetate in drinking water) on testes of weaned rats up to 90 days of age was investigated Histopathological examination of testes of lead treated rats maintained on low protein diet revealed marked pathological changes associated with greatly reduced succinic dehydrogenase, glucose-6-phosphate dehydrogenase and adenosine triphosphatase activity as revealed histochemically compared to lead treated rats fed normal protein diet. It was concluded that higher accumulation of lead may be responsible for altering the enzyme levels and inducing the testicular degeneration to a greater extent in low protein fed rats compared to their counterpart controls.

Animals↗
PubMed1989

Zinc protects testicular injury induced by concurrent exposure to cadmium and lead in rats.

The effect of coexposure to lead and cadmium (each 50 ppm alone and 25 ppm in combination) on the testes of rats and the preventive role of zinc (50 ppm) was investigated by administering these metals through drinking water. Male weaned albino rats were exposed to these metals for 120 days. Testicular histology, sperm counts and sperm motility were studied in these rats. The animals coexposed to lead and cadmium exhibited much more pronounced pathological changes and reduced sperm counts compared to the animals exposed to either of the metals alone. Zinc supplementation to the lead + cadmium exposed rats revealed the protective effect of zinc on these parameters. The observed higher magnitude of changes in the testes of lead + cadmium exposed group seems to be due to the excessive cadmium accumulation.

Animals↗
PubMed1989

Chronic cadmium-ethanol administration alters metal distribution and some biochemicals in rat brain.

The effects of cadmium (100 ppm through drinking water) and ethanol (5 g/kg by gastric gavage) administration on biogenic amines, metal distribution and certain enzymes in rat brain was investigated after 90 days of exposure. Co-exposure group revealed significant accumulation of cadmium and also increase in zinc levels compared to all the other groups. Ethanol alone decreased MAO activity and increased NE and 5-HT level while in combination with Cd, these effects were more magnified. It is, therefore, suggested that the persons consuming alcohol may be more prone to the neurotoxic effects of this metal.

Animals↗
PubMed1988

Testicular effects of acrylonitrile in mice.

Daily oral administration of acrylonitrile (10 mg/kg body weight) to mice for a period of 60 days caused a significant decrease in the activity of testicular sorbitol dehydrogenase and acid phosphatase, and an increase in that of lactate dehydrogenase and beta-glucuronidase. Histopathological studies revealed degeneration of the seminiferous tubules. A decrease in the sperm counts of the epididymal spermatozoa was also observed in the animals of the acrylonitrile-exposed group. These observations suggest that acrylonitrile may affect the male reproductive function by causing testicular injury.

Acid Phosphatase↗
PubMed1987

The effect of lead exposure on the testis of growing rats.

Daily intraperitoneal administration of lead (8 mg/kg) as lead acetate in male rats from 21 till 120 days of age triggered histopathological and biochemical alterations in the testis. Histopathological examination revealed disturbance in spermatogenesis besides Leydig cells degeneration. There was an increase in cholesterol, decrease in ascorbic acid contents and reduction in the glucose-6-phosphate dehydrogenase activity in the testis of lead-treated rats. These alterations suggest that the disturbed steroidogenesis during growing stage may be responsible for altering the germinal function of the testis at maturity.

Animals↗