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Biomedical subjects

S P Shukla

Publications and source records attributed to S P Shukla.

At least 19 recordsLinked to original sources
PubMed1992

Toxic effects of omega chrome red ME and its treatment by adsorption.

Toxic effects of Omega Chrome Red ME, a popular textile dye, on the nitrogen fixing cyanobacterium Nostoc calcicola were studied. The growth of N. calcicola was found to be suppressed at 10 and 20 mg liter-1 initial concentrations of dye, whereas a low initial concentration of 5 mg liter-1 slightly favors growth. Removal of the dye was carried out by adsorption using some cheap and unconventional adsorbents like coal, fly ash, wollastonite, and china clay. It has been observed that, in all cases, the low adsorbate concentration, the low temperature, and an acidic medium favor the dye removal process. The process of uptake follows first-order adsorption rate expression and obeys Langmuir's model of adsorption. The removal process is also partially diffusion controlled. Thermodynamic and pH studies were run to explain the results.

Adsorption↗
PubMed1990

Enzymatic and ultrastructural studies in a freshwater catfish: impact of methyl parathion.

Exposure to a sublethal concentration of methyl parathion (MEP) reduced the activity of cytoplasmic malate dehydrogenase, mitochondrial malate dehydrogenase, and lactate dehydrogenase by 30 to 49% in the liver and the skeletal muscle of the freshwater catfish. Clarias batrachus, after 7 days. The activities then began to recover and reached the control levels on the 28th day of MEP exposure. A complete recovery occurred on the 7th day when MEP was withdrawn from the medium after an exposure for 1 week. The withdrawal-dependent recovery in the activities was inhibited partially or completely by actinomycin D and cycloheximide, suggesting de novo synthesis of the enzymes during the recovery period. A conjoint treatment of MEP and triiodothyronine (T3) restored the activities to control levels, indicating T3 protection against the pesticide toxicity. SDS-PAGE of the cytoplasmic fraction of the liver showed some noticeable changes in the protein pattern after an exposure to MEP. Ultrastructural studies on MEP-treated liver cells showed disappearance of the glycogen granules and appearance of numerous smooth endoplasmic reticulum, lysosomal dense bodies, and swollen mitochondria. These changes in the liver are an indication of hepatic toxicity leading toward necrosis.

Animals↗
PubMed1990

Malate and lactate dehydrogenases of a freshwater catfish: impact of endosulfan.

A sublethal concentration of technical grade endosulfan (END) inhibited 35 to 55% of the activities of cytoplasmic malate dehydrogenase (cMDH), mitochondrial malate dehydrogenase (mMDH), and lactate dehydrogenase (LDH) in the liver and the skeletal muscle of a freshwater catfish, Clarias batrachus, after 7 days of exposure. The activity remained in the inhibited state up to 28 days. The withdrawal of END from the medium after 1 week of exposure gradually restored the activities to control levels within 21 days in the skeletal muscle and 28 days in the liver. The administration of actinomycin D or cycloheximide between the 14th and the 21st day of the withdrawal of END almost completely inhibited the withdrawal-dependent recovery in the activities of all the three enzymes. This indicates de novo synthesis of the enzymes during the recovery period. A conjoint treatment of END and triiodothyronine (T3) raised the activities of cMDH, mMDH, and LDH in the liver and the skeletal muscle up to the control levels. This shows that the inhibitory effect of END may be relieved in presence of T3. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed few changes in the pattern of cytoplasmic proteins of the liver and the skeletal muscle in response to exposure to END.

Animals↗
PubMed1988

Toxicity bioassay of technical and commercial formulations of carbaryl to the freshwater catfish, Clarias batrachus.

The acute toxicity of the carbamate insecticide, carbaryl, in technical and commercial formulations was investigated in the freshwater catfish, Clarias batrachus, after exposures of 24, 48, 72, and 96 hr. The "trimmed Spearman-Karber method" with 10% trimming was employed for the determination of median lethal concentration (LC(I)50). The LC(I)50 values of the commercial carbaryl (162.60, 134.08, 123.36, 107.66 mg/liter) decreased gradually with increase of exposure duration from 24, to 48, 72, and 96 hr, respectively. Similarly, the LC(I)50 values of technical grade carbaryl (61.14, 53.65, 48.58, 46.85 mg/liter) decreased with increasing length of exposure. This reflects a time-dependent adaptability of the fish to the toxicant. Further, the technical grade compound was 2.5 times more toxic than the commercial preparation. This demonstrates the involvement of carbaryl as the active principle in acute toxicity testing, rather than the additive substances. Dermal desquamation was observed as a characteristic change in response to carbaryl exposure.

Animals↗
PubMed1984

Regulation of pyruvate oxidation in blowfly flight muscle mitochondria: requirement for ADP.

Blowfly (Phormia regina) flight muscle mitochondria oxidized pyruvate ( + proline) in the presence of either ADP (coupled respiration) or carbonylcyanide-p-trifluoromethoxyphenylhydrazone (FCCP-uncoupled respiration). There was an absolute requirement for ADP (Km = 8.0 microM) when pyruvate oxidation was stimulated by FCCP in the presence of oligomycin. This requirement for ADP was limited to the oxidation of pyruvate; uncoupled alpha-glycerolphosphate oxidation proceeded maximally even in the absence of added ADP. Atractylate inhibited uncoupled pyruvate oxidation whether added before (greater than 99%) or after (95%) initiation of respiration with FCCP. In the presence of FCCP, oligomycin, and limiting concentrations of ADP (less than 110 microM), there was a shutoff in the uptake of oxygen. This inhibition of respiration was completely reversed by the addition of more ADP. Plots of net oxygen uptake as a function of the limiting ADP concentration were linear; the observed ADP/O ratio was 0.22 +/- 0.025. An ADP/O ratio of 0.2 was predicted if phosphorylation occurred only at the succinyl-CoA synthetase step of the tricarboxylate cycle. Experiments performed in the presence of limiting concentrations of ADP, and designed to monitor changes in the mitochondrial content of ADP and ATP, demonstrated that the shutoff in oxygen uptake was not due to the presence of a high intramitochondrial concentration of ATP. Indeed, ATP, added to the medium prior to the addition of FCCP, inhibited uncoupled pyruvate oxidation; the apparent KI was 0.8 mM. These results are consistent with the hypothesis that it is the intramitochondrial ATP/ADP ratio that is one of the controlling factors in determining the rate of flux through the tricarboxylate cycle. Changes in the mitochondrial content of citrate, isocitrate, alpha-ketoglutarate, and malate during uncoupled pyruvate oxidation in the presence of a limiting concentration of ADP were consistent with the hypothesis that the mitochondrial NAD + -linked isocitric dehydrogenase is a major site for such control through the tricarboxylate cycle.

Adenosine Diphosphate↗