Acute Toxicity of Carbofuran to a Freshwater Teleost, Clarias batrachus.
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Animals↗
Biomedical subjects
R L Singh
Publications and source records attributed to R L Singh.
High frequency of hepatitis B virus infection in patients with beta-thalassemia receiving multiple transfusions.
BACKGROUND AND OBJECTIVES: Hepatitis B virus (HBV) may occasionally be transmitted through transfusion of blood units that are hepatitis B surface antigen (HBsAg) negative but HBV DNA positive. Children with beta-thalassemia are particularly susceptible to HBV because they receive multiple blood transfusions. These children have high infection rates despite vaccination against HBV. Post-vaccination infections may be a result of viruses harbouring surface (S)-gene mutations (e.g. G587A) in a region critical for reactivity to antibody to hepatitis B surface antigen (anti-HBs). The true prevalence of HBV in individuals with beta-thalassemia has not been studied previously. PATIENTS AND METHODS: Seventy patients with beta-thalassemia (median age 6 years; range 8 months to 22 years; 49 male), who had received seven to 623 (median 61) units of blood each and three doses (10/20 micro g) of HBV vaccine (Engerix B) before presentation to us, were included in the study; 50 of the 70 patients had received transfusions prior to vaccination. Enzyme-linked immunoassay for serological markers [HBsAg, antibody to hepatitis B core antigen (anti-HBc) and quantitative anti-HBs] and polymerase chain reaction (PCR) followed by Southern hybridization for molecular detection of hepatitis B, was performed on all samples. The PCR-amplified product was cloned, sequenced and the nucleotide and deduced amino acid sequences for the HBV S and polymerase (P) genes were analysed for mutations. RESULTS: Four of 70 (5.7%) individuals with beta-thalassemia were HBsAg positive and 14 (20%) were anti-HBc positive. The prevalence of serological markers increased with number of transfusions (P < 0.01). Of 70 patients, 53 (75.7%) had an anti-HBs titre of > 10 IU/l following vaccination and 17 (24.3%) were non-responders (< 10 IU/l); 22 (31.4%) of the 70 were DNA positive. The frequency of HBV infection in beta-thalassemia was similar in vaccine responders and non-responders. The virus was of subtype ayw (genotype D) in the five DNA-positive samples in which a 388-nucleotide region of the S gene was sequenced. Mutations occurred at 13 positions in the S gene and at 10 positions in the P gene. Hydrophobicity plots revealed differences in amino acid regions 117-165 and 195-211. Some of these amino acid substitutions coincided with the putative cytotoxic T-lymphocyte epitopes of both S and P proteins. CONCLUSIONS: A high frequency of HBV infection was seen using molecular methods in thalassemic patients. The frequency of infection was similar in vaccine responders and non-responders. A number of mutations were observed in the S gene, which could have implications for viral replication as well as virus-host cell interaction.
Adolescent↗
Mode of action of acibenzolar-S-methyl against sheath blight of rice, caused by Rhizoctonia solani Kühn.
The mode of action of acibenzolar-S-methyl (BTH) was investigated against sheath blight of rice and its pathogen, Rhizoctonia solani. BTH exhibited limited fungitoxicity against R solani, in the form of reduced mycelial growth, hyphal browning and sclerotia formation. Parasite fitness of mycelia and sclerotia formed on BTH-amended media was also reduced. When applied as soil drench or foliar spray, BTH inhibited both disease development on inoculated sheaths and its spread to the younger sheaths. The degree of protection against sheath blight increased with increase in duration between BTH application and inoculation. The curative effect of BTH was poor. When applied through roots a protective effect of BTH was visible even with only a 1-h interval between application and inoculation. However, in the case of foliar application, protective effect was recorded only when the gap between application and inoculation was 24 h. BTH reduced the frequency of penetration by R solani, colonization of host tissue and spread of the hyphae from primary lesions to form secondary lesions. BTH induced swelling of hyphal tips on the sheath surface, formation of papillae, browning of penetrated epidermal cells and degeneration of intra-cellular hyphae colonizing epidermal and mesophyll cells. Therefore, the protective effect of BTH against sheath blight was due to combination of its host defence-inducing activity and its adverse effect on growth and vigor (parasite fitness) of the pathogen.
Dose-Response Relationship, Drug↗
Uptake and translocation of carpropamid in rice (Oryza sativa L).
Translocation of the antiblast compound, carpropamid, was investigated in rice using [14C]carpropamid. When applied to the seed, carpropamid was not only readily absorbed but was translocated to different parts of the seedlings emerging from treated seeds. A substantial portion of fungicide appeared to be exuded onto the leaf surface. In 21-day-old plants grown from [14C]carpropamid-treated seeds, 27.2% of the radioactivity isolated from leaves was present on the surface of lamina. This exuded fraction is probably responsible for its action as a fungal anti-penetrant compound. Following 30-min root dipping of 14-day-old seedlings, carpropamid was rapidly absorbed and translocated throughout the seedling. Its intra-laminar distribution was uniform as determined by autoradiography. Only a small fraction (< 2%) of fungicide applied to the foliage was translocated beyond the site of application within the treated leaf. Translocation was primarily apoplastic. Approximately 54% of the radioactivity recovered from leaves was in the form of carpropamid. At least seven radiolabelled metabolic products were observed by TLC. Only 8.3% of radioactivity applied through the seeds could be recovered from 21-day-old seedlings.
Amides↗
Artemisinin, an endoperoxide antimalarial, disrupts the hemoglobin catabolism and heme detoxification systems in malarial parasite.
Endoperoxide antimalarials based on the ancient Chinese drug Qinghaosu (artemisinin) are currently our major hope in the fight against drug-resistant malaria. Rational drug design based on artemisinin and its analogues is slow as the mechanism of action of these antimalarials is not clear. Here we report that these drugs, at least in part, exert their effect by interfering with the plasmodial hemoglobin catabolic pathway and inhibition of heme polymerization. In an in vitro experiment we observed inhibition of digestive vacuole proteolytic activity of malarial parasite by artemisinin. These observations were further confirmed by ex vivo experiments showing accumulation of hemoglobin in the parasites treated with artemisinin, suggesting inhibition of hemoglobin degradation. We found artemisinin to be a potent inhibitor of heme polymerization activity mediated by Plasmodium yoelii lysates as well as Plasmodium falciparum histidine-rich protein II. Interaction of artemisinin with the purified malarial hemozoin in vitro resulted in the concentration-dependent breakdown of the malaria pigment. Our results presented here may explain the selective and rapid toxicity of these drugs on mature, hemozoin-containing, stages of malarial parasite. Since artemisinin and its analogues appear to have similar molecular targets as chloroquine despite having different structures, they can potentially bypass the quinoline resistance machinery of the malarial parasite, which causes sublethal accumulation of these drugs in resistant strains.
Animals↗
Gastric M1 mucin, an early oncofetal marker of colon carcinogenesis, is encoded by the MUC5AC gene.
Gastric M1 mucin and the MUC5AC gene show a similar oncofetal expression in the colon. Our aim was to determine whether M1 mucin is the product of the MUC5AC gene. A recombinant baculovirus encoding the C-terminal portion of the MUC5AC gene as a fusion protein was isolated and the immunoreactivity of the recombinant mucin (rM) toward M1 antibodies studied. Chicken antibodies also were raised against purified rM. Besides its reactivity with L56/C, a serum recognizing the bacterially expressed MUC5AC gene product, rM was endowed with M1 immunoreactivity: (i) rM-expressing cells were stained specifically with anti-M1 serum and with the monoclonal antibody (MAb) 21M1, defining the M1-f epitope; (ii) both L56/C and anti-M1 antibodies recognized the same bands in immunoblots of rM-containing cell extracts; (iii) the 21M1 antibody reacted with rM in an immunoradiometric assay. Among the 7 M1 epitopes, M1-f was the only one encoded by the 3' portion of the MUC5AC gene. It was the only epitope detected in a native mucin M1-derived 170 kDa bromelain proteolytic fragment. Furthermore, the staining patterns of human tissues obtained with either anti-rM chicken antibodies or anti-M1 antibodies were identical. We conclude that M1 immunoreactivity is encoded at least in part by the MUC5AC gene.
Animals↗
Effect of protein malnutrition on sex organs of metanil yellow exposed male rats.
Oral administration of metanil yellow (MY) at 3.0% (w/w) dose level to adult male albino rats maintained on low protein (LP) diet for 30 days resulted in a greater decrease in absolute and relative weights of testes than in those rats maintained on a normal protein (NP) diet. A marked decrease in the activities of lactate dehydrogenase and hyaluronidase and content of lactic acid in LP + MY fed animals suggested that low protein diet enhanced the vulnerability of germ cells towards metanil yellow. The lack of significant changes in the cholesterol content of testis, the fructose content of the coagulating glands and the dorso-lateral prostate, the activities of alkaline phosphatase in the seminal vesicle, and acid phosphatase in ventral prostate of the MY treated animals suggested that their androgenic status were not affected.
Acid Phosphatase↗
Synthetic peptides corresponding to a repetitive sequence of malarial histidine rich protein bind haem and inhibit haemozoin formation in vitro.
Synthetic peptides containing a repetitive hexapeptide sequence (Ala-His-His-Ala-Ala-Asp) of malarial histidine-rich protein II were evaluated for binding with haem in vitro. The pattern of haem binding suggested that each repeat unit of this sequence provides one binding site for haem. Chloroquine inhibited the haem-peptide complex formation with preferential formation of a haem chloroquine complex. In vitro studies on haem polymerisation showed that none of the peptides could initiate haemozoin formation. However, they could inhibit haemozoin formation promoted by a malarial parasite extract, possibly by competitively binding free haem. These results indicate this hexapeptide sequence represents the haem binding site of the malarial histidine-rich protein and possibly the site of nucleation for haem polymerisation.
Amino Acid Sequence↗
P-aminodiphenylamine induced biochemical changes in sex organs of male albino rats.
Intraperitoneal administration of p-aminodiphenylamine (p-ADPA), an aromatic amine of wide industrial applications, / 42.5 mg/kg body weight for 180 days significantly decreased the activities of testicular lactate dehydrogenase and hyaluronidase and lactic acid content indicating arrest of spermatogenesis. Patchy necrosis of the testis was confirmed histopathologically. No change in testicular cholesterol, fructose content of coagulating glands and dorso-lateral prostate and activities of alkaline phosphatase in seminal vesicle and acid phosphatase in ventral prostate support normal androgenic status.
Animals↗
Metabolic disposition of 14C-metanil yellow in guinea pigs.
The absorption, metabolism and excretion of 14C-metanil yellow was studied in guinea pigs. Following administration of a single po dose of 5 mg dye (7.6 mu Ci)/kg body weight, 83.4% was excreted through urine and feces within 96 h with the majority accounted for in feces. Liver, kidney and spleen did not have marked accumulation of counts, whereas testes and gastrointestinal tract retained 1.9 and 9.7% of the radioactivity, respectively. Analysis of urine and feces detected 2 azo-reduction metabolites of metanil yellow which were characterized by TLC and IR, NMR and mass spectroscopic studies as metanilic acid and p-aminodiphenylamine.
Animals↗
Metabolic disposition of [14C] metanil yellow in rats.
The absorption, metabolism and excretion of [14C] metanil yellow was studied in rats. Following administration of a single oral dose of 5 mg dye (7.6 microCi)/kg body weight, 80.5% of the dose was excreted in the urine and faeces within 96 hr, with the majority being accounted for in the faeces. Liver, kidney, spleen and testis retained no count whereas 13.6% of the radioactivity was retained by gastrointestinal tract. Analysis of urine and faeces detected two azo-reduction metabolites of metanil yellow which were characterized by TLC and IR, NMR and mass spectroscopic studies as metanilic acid and p-aminodiphenylamine.
Animals↗
Potential CNS active agents. II--Studies of 4(3H)-quinazolinones.
Some new 2-carbamoylmethylthio- and 2-(omega-dimethylamino-alkyl)thio-3-aryl-7-chloro-4(3H)-quinazolinones have been prepared from 2-thio-3-aryl-7-chloro-4(3H)-quinazolinones as the key intermediate. Five of the synthetic compounds were screened for their CNS activities on mice and found to be either CNS depressants or stimulants.
Animals↗
Acute and short-term toxicity of a popular blend of metanil yellow and orange II in albino rats.
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Animals↗
Acute and short-term toxicity studies on orange II.
Inspite of its non-inclusion in the prescribed list of food colors, orange II is extensively employed to color a variety of foodstuffs. Oral LD50 value of orange II in both male and female rats was calculated to be more than 10.56 g/kg body weight. In short-term studies, animals were exposed to diets containing 0.0 (control), 0.1, 0.5 or 3.0% (w/w) of orange II, daily for 90 days. Hematological examination revealed a slight decrease in erythrocyte count and hemoglobin content, whereas leucocyte count, PCV, ESR, MCV, MCH and MCHC showed normal values. There was no change in the activities of LDH, GOT, GPT, alkaline/acid phosphatases and bioconstituents, lactic acid, cholesterol and protein in serum as well as in liver, indicating normal functioning of the liver. Histopathological examination of various body organs such as liver, heart, lung, kidney, testes, adrenal, stomach, large and small intestine presented normal appearance. Animals receiving 3.0% orange II showed marked splenomegaly and deposition of Perl's positive iron pigments. Testicular LDH, hyaluronidase and lactic acid did not reveal any deviation from controls, suggesting normal spermatogenic process. No changes in testicular cholesterol, fructose content of coagulating glands and dorso-lateral prostate, and activities of alkaline phosphatase in seminal vesicle and acid phosphatase in ventral prostate support normal androgenic status.
Animals↗
Acute and short-term toxicity studies on p-aminodiphenylamine.
p- Aminodiphenylamine (p-ADPA), an aromatic amine of wide industrial applications, also finds human exposure through hair dye preparations or via ingestion of a common food colouring metanil yellow. Acute and short-term toxicity studies in albino rats have been done following the biochemical markers, hematology and tissue histopathology. The acute LD50 value of p-ADPA is 0.847 g/kg body weight which qualifies for the 'moderately toxic' category. In short-term studies, animals were fed p-ADPA, mixed in routine laboratory diet at the concentrations of 0.0 (control), 0.1, 0.25, 0.5 and 0.75% (w/w), daily for 90 days. Feed intake and body weight gain in the highest dosed group were reduced. Hematological examinations exhibited moderate anemic conditions with decreased red blood cells, increased erythrocyte sedimentation rate and lowered packed cell volume suggesting normocytic normochromic anemia at 0.25% onward levels of p-ADPA intake. There was significant increase in the activities of acid/alkaline phosphatases and GOT/GPT in serum with simultaneous depletion from liver at the levels of 0.5 and 0.75% p-ADPA intake, suggesting biochemical lesions of the liver. Testicular LDH and hyaluronidase were lowered at 0.5 and 0.75% levels indicating partial arrest of spermatogenesis. These findings were supported histopathologically. The study warrants careful consideration on its exposure, industrially or through common food color or hair dye preparations.
Anemia↗
Age at first calving and its relation to first lactation yield in Bachaur cattle.
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Age Factors↗
Observations on Bachaur cattle.
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Animals↗
Frequency of infection by hepatitis B virus and its surface mutants in a northern Indian population.
INTRODUCTION: The reported prevalence of hepatitis B virus (HBV) infection in the Indian general population varies from 2% to 11%. Epidemiological studies conducted so far have selection biases, since these included populations of defined age group, gender, social class, high-risk group, etc. The present study was designed to look for the molecular epidemiology of HBV infection in the rural and urban general populations in India. METHODS: Sera obtained from healthy volunteers during college and social service camps from parts of northern India were tested for HBsAg and anti-HBc using enzyme immunoassays and for HBV DNA using polymerase chain reaction and Southern blot hybridization. The amplification products were cloned and sequenced, and nucleotide and deduced amino acid sequences of the surface and polymerase genes were analyzed for mutations. RESULTS: Of the 730 subjects (rural 543, urban 187), 15 (2.1%) tested positive for HBsAg and 143 (19.5%) for anti-HBc; 10 were positive for both. The overall HBV exposure rate in the population was 20.3% (148/730). The HBsAg carrier rate was similar in the urban and rural populations (1.5% and 2.3%; p=ns), and anti-HBc positivity was lower in the urban population (8.5% vs. 23.3%; p<0.01). History of parenteral interventions or blood transfusion was associated with markers of exposure to HBV (10.2% vs. 4.6%; p=0.01). Among the 220 representative samples tested for HBV DNA, 14 (6.4%) were positive; of these, only four were positive for HBsAg or anti-HBc. Sequencing of a 388-nt segment of the S-gene from three individuals (two adw and one ayw subtype) revealed four mutations. Two and three of these led to amino acid changes in the HBV surface and polymerase genes, respectively; alterations in known cytotoxic T cell epitopes of HBV surface and polymerase proteins were observed in one individual each. None had the G587A mutation, which is known to be associated with loss of the 'a' determinant of HBsAg. CONCLUSION: Our study shows a high frequency of exposure to HBV infection in the Indian general population; a proportion of HBV infected persons were detectable only by molecular methods. The positivity rate was higher in the rural population.
Adolescent↗