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Biomedical subjects

R C Murthy

Publications and source records attributed to R C Murthy.

At least 19 recordsLinked to original sources
PubMed2006

Effect of fly ash inhalation on biochemical and histomorphological changes in rat liver.

The effect of fly ash inhalation (4h daily, 5 days a week) for 28 days on the deposition of metal ions and histopathological changes in the liver and serum clinical enzymes has been studied. The results showed an increase in the concentration of metals such as cadmium (Cd), chromium (Cr), copper (Cu), manganese (Mn), and lead (Pb) in the tissues of exposed rats. The level of metals varied from metal to metal and from organ to organ. Level of serum enzymes such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, and alkaline phosphatase were increased in fly ash exposed rats using whole body inhalation exposure as compared to sham controls. Histopathological studies of rat liver exposed to fly ash revealed infiltration of mononuclear cells in and around the portal triads, which seems to be laden with fly ash particles. Hepatocytes showed necrotic changes such as pyknotic nuclei, karyorrhexis, and karyolytic. These changes were more towards the centrolobular areas than the midzonal and periportal areas. These findings demonstrate that the toxic metals of inhaled fly ash in rats may get translocated into extrapulmonary organs, become deposited and hence may manifest their toxic effects on different tissues.

Alanine Transaminase↗
PubMed2005

Comparative biomonitoring of leachates from hazardous solid waste of two industries using Allium test.

Hazardous industrial wastes are inevitable source of environmental pollution. Leachates from these wastes might contaminate the origins of potable water and affect human health. The study was carried out to determine the possible genotoxic effects of leachates from solid waste of a metal and dye industry using the Allium cepa chromosome aberrations assay. The 10% leachates were prepared from solid wastes obtained from both the industries and examined for the presence of heavy metal content and genotoxicity. To simulate the field and laboratory conditions, A. cepa bulbs were exposed through soil and aqueous medium for 48 h to 2.5-10% leachates. The results revealed that both metal waste leachate (MWL) and dye waste leachate (DWL) contained high concentrations of chromium, nickel and iron that significantly induced cytogenetic alterations. Significant inhibition of mitotic index (MI), inductions of chromosomal/mitotic aberrations (CA/MA) and micronuclei (MN) formation were found in all experimental groups exposed to MWL and DWL. The effects observed were concentration dependent and the frequency of aberrations was higher with treatment of MWL than DWL. The MI was severely inhibited at 10% aqueous exposure it was 4.59+/-0.69 (P<0.001) in MWL and almost half to that induced by DWL that was 8.62+/-0.69 (P<0.05). Significant frequency of CA/MA and MN induced by MWL was 14.21 (P<0.001) and 0.33 (P<0.001) whereas CA/MA and MN induced by DWL was 7.81 (P<0.001) and 0.13 (P<0.05) in the aqueous medium. The investigations inferred that abnormalities caused by MWL were higher than DWL both in soil and aqueous media. These toxic responses may have relied on raised heavy metal concentrations of metal-based than dye industrial wastes.

Chromosome Aberrations↗
PubMed2005

Genotoxicity of industrial solid waste leachates in Drosophila melanogaster.

The potential toxicity of industrial solid wastes is a major environmental concern. The present study evaluated the genotoxicity of industrial waste leachates on the gut cells of Drosophila melanogaster (Oregon R+), using a modified alkaline comet assay. Leachates were prepared from control soil and solid wastes generated by a flashlight battery factory, a pigment plant, and a tannery, using different pHs (7.0, 4.93, and 2.88). Newly emerged first instar Drosophila larvae (22 +/- 2 hr) were transferred to standard Drosophila diet containing 0.05%, 0.1%, 0.5%, 1.0%, and 2.0% of the leachates, and allowed to grow. At 96 +/- 2 hr, the anterior midgut of control and treated larvae was dissected out; single cell suspensions were prepared; and the comet assay was performed on the cells. All the leachates produced significant (P < 0.05), dose-dependent increases in DNA damage, in the gut cells. Leachates prepared at pH 7.0 were significantly less genotoxic than leachates prepared at pH 4.93 or 2.88. A comparison of the comet parameters among the exposed groups indicated that leachates of the pigment plant solid waste produced the least DNA damage, while leachates prepared from the flashlight battery factory solid waste were the most genotoxic. The present study indicates that leachates of solid wastes from flashlight battery factories, pigment plants, and tanneries possess genotoxic activity and that D. melanogaster is a useful in vivo model for assessing the genotoxicity of these potential environmental contaminants.

Animal Feed↗
PubMed2004

Modulation of flyash-induced genotoxicity in Vicia faba by vermicomposting.

Cytogenetic effects of pre- and postvermicomposted flyash samples were evaluated on the root meristem cells of Vicia faba. Seedlings of V. faba were directly sown in flyash and cow dung-soil mixtures (20%, 40%, 60%, and 80%) and the lateral roots grown in these test mixtures were sampled at 5 days. Negative control was run parallel in cow dung-soil (CS) mixture alone. One set of flyash-cow dung-soil (FCS) mixture was subjected to vermicomposting by introducing Eisenia foetida species of earthworms for 30 days and the cytogenetic effects were reinvestigated through V. faba root meristems. Chemical analysis carried out prior to vermicomposting revealed high concentrations of heavy metals such as Cr, Cu, Pb, Zn, and Ni in FCS samples. CS samples also showed the presence of these metals. Cytogenetic examinations of root meristems exposed to the FCS mixtures showed significant inhibition of mitotic index (MI), induction of chromosome aberrations (CA), and a significantly increased frequency of mitotic aberrations (MA). The increase of the aberrations was dependent on the flyash concentrations. Roots grown in CS samples also showed chromosomal and MAs; however, the percentage was lower than that observed with FCS and also statistically nonsignificant. Cytogenetic analysis of vermicomposted samples of FCS revealed a 15-45% decline in the aberration frequencies whereas chemical analysis showed a 10-50% decline in the metal concentrations, viz. Cr, Cu, Pb, Zn, and Ni, which indicates E. foetida a potential accumulator of heavy metals and the decline in metal concentrations may be the cause of the decrease in aberration frequencies. The present study indicates the genotoxicity potential of flyash and also the feasibility of vermicomposting for cleanup of metal-contaminated soil to mitigate the toxicity/genotoxicity.

Animals↗
PubMed2004

Male reproductive toxicity of sodium arsenite in mice.

The effect of chronic oral exposure to arsenic on male mouse testicular and accessory sex organ weights, sperm parameters and testicular marker enzymes was studied. In addition, the distribution of arsenic in reproductive organs was measured using atomic absorption spectrophotometry. Sodium arsenite administered to mice (Mus musculus) via drinking water at a dose of 53.39 micromol/L (4 ppm As) for 365 days caused a decrease in the absolute and relative testicular weight. However, epididymal and accessory sex organ weight was similar to control. The activities of marker testicular enzymes such as sorbitol dehydrogenase, acid phosphatase and 17beta-hydroxy-steroid dehydrogenase (17beta-HSD) were significantly decreased, but those of lactate dehydrogenase and gamma-glutamyl transpeptidase (gamma-GT) were significantly increased. A decrease in sperm count and sperm motility, along with an increase in abnormal sperm, was observed in arsenite-exposed mice. A significant accumulation of arsenic in testes, epididymis, seminal vesicle and prostate gland was observed in treated animals. Thus long term exposure (365 days) at the dose level of 53.39 micromol/L sodium arsenite (4 ppm As), to which human beings are likely to be exposed via drinking water, may cause testicular and spermatotoxic effect.

Administration, Oral↗
PubMed2002

Neuropsychological studies on lead battery workers.

This study assessed the psychological status of 60 lead-acid battery workers occupationally exposed to low level lead and 30 referents in Lucknow. Digit spans and symbol, Bourdon-wiersma vigilance and Raven's Progressive matrices tests were administered. Significant impairments in concentration, attention, auditory and visual memory, psycho-motor speed, perceptual accuracy, and visual reasoning were observed in the workers compared to the referents. The deficits were not related to exposure duration since the magnitude of the impairments observed in workers with 1-y duration was the same as in those with more (up to 30 years) work duration. The blood lead of the battery workers was significantly elevated. There were functional deficits of the central nervous system in the lead-acid battery workers.

Adolescent↗
PubMed2001

Male reproductive effect of arsenic in mice.

Arsenic, a known human carcinogen, was given to mice via drinking water as sodium arsenite at a dose 53.39, 133.47, 266.95 and 533.90 micromol 1 for 35 days. A decrease in the activity of 17 beta HSD along with increase in LDH, gammaGT activity were observed at 533.90 micromol l. The observed sperm count, motility and morphological abnormalities in sperm were similar to control at lower dose levels. However at 533.90 micromol l a significant decrease in sperm count and motility along with increase in abnormal sperm were noticed. Significant accumulation of arsenic in testes and accessory sex organs may be attributed to the arsenic binding to the tissues or greater cellular uptake. No effects were observed on indices studied for reproductive effects at 53.39 micromol l arsenic close to which human being are exposed through drinking water under the present set of experimental conditions.

Animals↗
PubMed1999

Effect of cadmium on the hatching of Metaphire posthuma cocoons.

Earthworms are considered ideal soil organisms for use in terrestrial ecotoxicology. Due to their susceptibility of heavy metals, the effect of cadmium on the hatching of M. posthuma cocoons was studied. The hatching was observed by the water incubation method and the doses of Cd were 0, 1.25, 2.5, 5.0, 10.0 and 40.0 ppm. The 0 and 1.25 ppm treated cocoons hatched within 45-60 days at 20 degrees C with 80% hatching rate and one juvenile per cocoon; no hatching was observed at higher concentrations. Furthermore, there was a linear increase in Cd residue in the treated cocoons. These results are apparently ill effects of Cd on embryonic development of the earthworms.

Animals↗
PubMed1998

Embryo and fetotoxicity of hexavalent chromium: a long-term study.

Ingestion of chromium(VI) (250, 500 or 750 ppm as potassium dichromate, K2Cr2O7) through drinking water by female rats for 3 months prior to gestation was toxic to embryo and fetus. There was a significant reduction in number of implantations and number of fetuses and an increase in number of resorptions and pre-implantation and post-implantation losses. No significant visceral abnormality was found. The increase in the number of subdermal hemorrhagic patches on the thorax and abdomen was significant. Skeletal abnormality in the form of reduced ossification in parietal, interparietal and caudal bones was observed in fetuses. Chromium levels in the blood of mothers, placenta and fetuses showed a significant increase. Duration of the estrous cycle was also increased significantly. The study revealed that long-term chromium exposure in rats did not cause embryo and fetotoxicity in a duration-dependent manner compared to short-term treatment as observed earlier. A possible explanation could be that, in the 90-day study, the female rats did not mate for three estrous cycles, thus giving time for clearance of a sizable amount of chromium from their bodies.

Abnormalities, Drug-Induced↗
PubMed1998

Role of iron and copper during benzene toxicity.

Role of transition metal ions in expression of benzene toxicity has been suggested. Intraperitoneal administration of benzene to female albino rats daily for 10 days resulted in accumulation of iron in liver nuclei, without any change in copper content. Incubation of hydroquinone (HQ), one of the principal metabolites of benzene with rat liver nuclei resulted in formation of thiobarbituric acid reactive products (TBAR). However, presence of bathocuproine, a copper chelator and EDTA, an iron chelator caused significant inhibition of TBAR release. Thus, the present study revealed that iron accumulation and involvement of copper in nuclear damage induced by HQ.

Animals↗
PubMed1996

Chromium induced teratogenicity in female rat.

Exposure to chromium (VI) (250, 500 and 750 ppm as potassium dichromate) via drinking water pregestationally in rats revealed embryo- and fetotoxic effects in the form of a significant reduction in the number of implantations and number of fetuses. An increase in the number of resorptions, pre-implantation and post-implantation loss in chromium (VI)-treated mothers was also observed. No significant visceral abnormality was found. A significant increase in sub-dermal hemorrhagic patches on thoracic and abdominal areas was found. Skeletal abnormality in the form of reduced ossification in parietal, interparietal and caudal bones was found in the fetuses of chromium (VI)-treated mothers. Chromium levels in blood, placenta and fetuses were found to be significantly increased in the 500 ppm and 750 ppm dosed groups. The duration of estrus cycle was significantly altered after chromium (VI) exposure. This study suggests that chromium exposure in rat causes a lower degree of toxicity than in mice as observed in our earlier studies.

Abnormalities, Drug-Induced↗
PubMed1996

Ovarian dysfunction in mice following chromium (VI) exposure.

Chromium (VI) was given through drinking water in two sets of adult Swiss albino female mice in three doses; 250 ppm, 500 ppm and 750 ppm for 20 days in set 1 and 0.05 ppm, 0.5 ppm and 5.0 ppm in set II for 90 days. At the termination of the treatment, the animals of both the sets were euthanized for histopathology, follicle counting, counting of the superovulated ova, duration of estrus cycle and for ultrastructural studies. Ovaries of the highest dose group (750 ppm) showed large numbers of atretic follicles and congestion in stromal tissue compared to the rest of the treated groups. Also, there was a dose-dependent reduction in the number of follicles at different stages of their maturation. The number of ova recovered from superovulated chromium (VI)-treated animals showed significant decreases in the 500 and 750 ppm dosed groups compared to lower dosed (250 ppm) and control groups. The duration of estrus cycle increased in highest dosed (750 ppm) group. A dose-dependent increase in blood chromium level was also seen in treated mice. Ultrastructural observations revealed disintegrated cell membranes of two layered follicular cells and altered villiform mitochondria in thecal cells of 5 ppm dosed group. From the study it was concluded that ovarian physiology and rate of ovulation might be altered if females are exposed to sufficiently high chromium through oral route.

Administration, Oral↗
PubMed1996

Cattle mortality in the Thane district, India: a study of cause/effect relationships.

An unexpected mortality of more than 300 cattle was investigated near a metal recovery factory located in a rural area of the Thane district of India. The factory was engaged in reclaiming lead, aluminum, tin, and zinc from discarded lead storage batteries and soft drink cans. The environmental samples (soil, leaves, grass, slag, water, and sediment), human blood and hair and animal samples (blood, urine, peritoneal fluid, liver, kidney, cow dung, ribs, and femur), collected for analysis revealed toxic levels of lead, cadmium, and chromium. Clinical examination of factory workers and school children revealed cough, fever, gastric problems, abdominal pain, skin lesions (scabies), and blue line on gums. Histopathological examination of animal tissues revealed chronic pathology with lead inclusion bodies in hepatocytes and renal tubules. Based on environmental, clinical, analytical, and histopathological observations, the mortality has been attributed to toxic levels of metals in the body and the malnourished status of the animals.

Adolescent↗
PubMed1996

Embryotoxicity of orally administered chromium in mice: exposure during the period of organogenesis.

Administration of chromium (VI)(250, 500 and 750 ppm as potassium dichromate) via drinking water during organogenesis (days 6-14 of gestation) in mice revealed embryo- and fetotoxic effects. Reduced fetal weight, retarded fetal development, number of fetuses (live and dead) per mother and high incidences of dead fetuses and resorptions in treated mothers in the highest dosed group were evident. No significant gross structural abnormalities were observed in any of the fetuses of chromium (VI)-treated mothers. Significant incidences of reduced ossification were found in the highest dosed group. Chromium levels were increased in a dose-dependent manner in maternal blood, placenta and fetuses. The present study suggests a risk to the developing embryo if the mother is exposed to a sufficiently high concentration of chromium (VI) through drinking water during the period of organogenesis.

Abnormalities, Drug-Induced↗
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↗
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↗