Hypotonic swelling-induced Ca2+ release by an IP3-insensitive Ca2+ store

Hypotonicswelling increases the intracellular Ca²⁺ concentration([Ca²⁺]_i) in vascular smooth muscle cells(VSMC). The source of this Ca²⁺ is not clear. To study thesource of increase in [Ca²⁺]_i in response tohypotonic swelling, we measured [Ca²⁺]_i infura 2-loaded cultured VSMC (A7r5 cells). Hypotonic swelling produced a40.7-nM increase in [Ca²⁺]_i that was notinhibited by EGTA but was inhibited by 1 µM thapsigargin. Priordepletion of inositol 1,4,5-trisphosphate (IP₃)-sensitive Ca²⁺ stores with vasopressin did not inhibit the increasein [Ca²⁺]_i in response to hypotonic swelling.Exposure of ⁴⁵Ca²⁺-loaded intracellular storesto hypotonic swelling in permeabilized VSMC produced an increase in⁴⁵Ca²⁺ efflux, which was inhibited by 1 µMthapsigargin but not by 50 µg/ml heparin, 50 µM ruthenium red, or25 µM thio-NADP. Thus hypotonic swelling of VSMC causes a release ofCa²⁺ from the intracellular stores from a novel sitedistinct from the IP₃-, ryanodine-, and nicotinic acidadenine dinucleotide phosphate-sensitive stores.

     

Nitrogen fixation and indole acetic acid production by Azospi-rillum sp. as influenced by an insecticide, carbofuran

Both indole acetic acid (IAA) accumulation and nitrogen fixation were increased in Azospirillum cultures isolated from rice roots and soils by carbofuran (2, 3-dihydro-2, 2-dimethyl-7-benzofuranyl-N-methyl carbamate), an insecticide widely used in rice cultivation. Addition of carbofuran at 5 and 10 parts/10₆ significantly stimulated nitrogen fixation in Azospirillum. Indole acetic acid accumulation by Azospirillum cultures was more pronounced at a lower level (250 g/50 ml) of carbofuran. Evidence is provided for carbofuran degradation by Azospirillum cultures. The 7-benzofuranol (2, 3-dihydro-2–2-dimethyl-7 benzofuranol), a major degradation product of carbofuran, however, did not enhance the IAA accumulation. The higher accumulation of IAA in Azospirillum in the presence of carbofuran is probably related to the increased growth due to fixed N present in the insecticide. Results indicate the involvement of parent compound carbofuran and/or compounds other than the 7-benzofuranol in the higher accumulation of IAA by Azospirillum sp.     

Changes in UsnRNA biosynthesis during rat liver regeneration

Partial hepatectomy (P.H.) induces a partially synchronized growth response of liver under normal regulation of growth. In this phase changes in cellular morphology, radial distribution pattern of cells and other biological as well as major biochemical changes are well documented [24]. Here, we have shown that the cellular content of UsnRNAs altered during this proliferative phase as well. The level of spliceosomal UsnRNAs (U1, U2, U4–U6) gradually decreased by 30–50% upto 48 hrs of P.H. followed by gradual increase to reach the normal level within one month of P.H. The U3 snRNA level on the other hand, was nearly equal to that in normal liver at 48 hrs of P.H. but in 24 and 72 hrs of P.H. its level was high (4 fold) in contrast to that in other UsnRNAs. Thus, it is clear from our data that the level of all the six UsnRNAs decreased during 48 hrs of P.H. compared to that after first 24 hrs. This has been correlated in the kinetics of UsnRNAs' synthesis (in terms of labelling) in isolated hepatocytes, where the rate of labelling of all the six UsnRNAs increased 20–30% in 24 hrs regenerating hepatocytes (R.H.) followed by sharp decrease by 30–50% within next 24 hrs, compared to that in the normal hepatocytes. But from 72 hrs onwards in R.H. the rate of labelling of all the six UsnRNAs again increased by 30–50% (compared to that in normal hepatocytes) followed by decrease of their labelling-rate to reach the normal level in R.H. within one month of P.H. Thus, it may be concluded that the changes in UsnRNAs' level during the proliferative phase of liver regeneration may be either due to the alteration in the rate of synthesis (in terms of labelling) or along with it differential turn over rate; this phenomenon may have some consequences with the regenerative process of liver.This paper was published in Molecular and Cellular Biochemistry131:67–73, 1994. Kluwer Academic Publishers regret the publication of the only partly corrected version.     

Composition and dynamics of epilithic algae in a forest stream at Shillong (India)

The seasonal dynamics of epilithic algae in a third order pristine forest stream were analyzed over a period of 2 years. Stream water was slightly acidic and nutrient poor. Encrusting, filamentous flocs, and filaments were found. Algal standing crop was high (mean concentration of Chl a 16–43 mg m^–2) in spring. Filamentous algae contributed most to standing crop. Diatoms made up over 85% by number of the epilithon. Blue-greens were abundant upstream, and chlorophytes downstream. This shift was ascribed to greater light availability downstream. The community was more diverse during spring. Water current was the most important variable regulating epilithon structure. Total phosphorus (TP), orthophosphate (O-PO _inf4 ^su3– ), silica (Si⁴⁺), nitrate (NO _inf3 ^su– ) and conductance correlated negatively with flow rate. Green algae showed a positive correlation to phosphorus during low and stable flow. During rapid runoff, diatoms were the most resistant forms. Seasonal change in the epilithic community was mainly regulated by fluctuations in flow rate.     

Hydroxylamine inhibition of the nitrate reductase complex from Amaranthus

Nitrate reductase from Amaranthus viridis is similar to nitrate reductase from other plant sources. NH₂OH inhibits nitrate reduction from NADH by the nitrate reductase complex, but it does not inhibit either the NADH-dehydrogenase activity or nitrate reduction from reduced flavin mononucleotides. The inhibition observed was non-competitive with nitrate when the enzyme was pre-incubated with NH₂OH and NADH, and competitive with nitrate without pre-incubation. The K_i values for NH₂OH were 5 μM and 30 μM with or without pre-incubation respectively.     

The influence of thick floating vegetation (Water hyacinth: Eichhornia crassipes) on the physico — chemical environment of a fresh water wetland

Measurements made in fresh water wetland have shown that temperature, pH, dissolved oxygen and bicarbonate alkalinity in the hyacinth infested area were lower, but dissolved free carbon dioxide concentration was excitingly greater than in the open water area. This extreme hypoxic and hypercarbic condition of hyacinth covered areas was caused by the thick coverage of Eichhornia crassipes which was crucial for the composition of the characteristic flora and fauna.     

Dimethyl fumarate protects thioacetamide‐induced liver damage in rats: Studies on Nrf2, NLRP3, and NF‐κB

The present study was designed to investigate the hepatoprotective potential of dimethyl fumarate (DMF) against thioacetamide (TAA)‐induced liver damage. Wistar rats were treated with DMF (12.5, 25, and 50 mg/kg/day, orally) and TAA (200 mg/kg intraperitoneally, every third day) for 6 consecutive weeks. TAA exposure significantly reduced body weight, increased liver weight and index, and intervention with DMF did not ameliorate these parameters. DMF treatment significantly restored TAA‐induced increase in the levels of aspartate aminotransferase, alanine aminotransferase, γ‐glutamyl transferase, total bilirubin, uric acid, malondialdehyde, reduced glutathione, and histopathological findings such as inflammatory cell infiltration, deposition of collagen, necrosis, and bridging fibrosis. DMF treatment significantly ameliorated TAA‐induced hepatic stellate cell activation, increase in inflammatory cascade markers (NACHT, LRR, and PYD domains‐containing protein 3; NLRP3, apoptosis‐associated speck like protein containing a caspase recruitment domain; ASC, caspase‐1, nuclear factor‐kappa B; NF‐κB, interleukin‐6), fibrogenic makers (α‐smooth muscle actin; ɑ‐SMA, transforming growth factor; TGF‐β1, fibronectin, collagen 1) and antioxidant markers (nuclear factor (erythroid‐derived 2)‐like factor 2; Nrf2, superoxide dismutase‐1; SOD‐1, catalase). The present findings concluded that DMF protects against TAA‐induced hepatic damage mediated through the downregulation of inflammatory cascades and upregulation of antioxidant status.