Biomedical subjects

H Huang

Publications and source records attributed to H Huang.

At least 361 records · Page 20Linked to original sources

PubMed1998

[Receptor-mediated endocytosis induced macrophage cytosolic acidification and exocytosis].

The effects of Con A, WGA, Zymosan A on macrophage cytosolic pH and outflow of lysosomal content through exocytosis were studied with SNAFL-calcein and FITC-Dextran on ACAS570. The results showed all three ligands could induce macrophage cytosolic acidification in about 10 min and kept at the same level hereafter; outflow of lysosomal fluorescent probe through exocytosis appeared in 15-20 min. In resting conditions, macrophage lysosomes mainly distributed in cell center; after stimulated for 15 min by three ligands, the number of lysosomes increased in membrane periphery, in 25-30 min lysosomes moved back toward cell center. We proposed that ligands induced lysosomal pH rises was a basic factor for outflow of lysosomal content through exocytosis, cytosolic acidification inhibited receptor-mediated endocytosis. Cytosolic acidification and outflow of lysosomal content through exocytosis were the results of cellular self-regulation and self-protection during receptor-mediated endocytosis.

Animals↗

PubMed1998

[Comparison of roxithromycin bioavailability of a conventional and a dispersible tablet formulation].

Following oral administrations of a single dose of 150 mg roxithromycin dispersible tablet (formulation A, a new formulation for clinical trial) and conventional tablet (formulation B, purchased from the market) to each of 10 healthy male volunteers in a randomized crossover design, the plasma levels of active drug at different times were determined by a microbial assay with Micrococcus luteus CMCC (B) 28001 and the plasma concentration-time profiles were obtained. The Tmax values of formulation A and B obtained were 1.7 +/- 0.9 and 3.7 +/- 1.6 h, the Cmax values were 4.97 +/- 1.17 and 2.04 +/- 1.26 micrograms.ml-1 and the AUC0-->infinity values were 62.2 +/- 11.9 and 35.0 +/- 16.9 micrograms.h.ml-1, respectively. Surprisingly, the relative bioavailability of formulation B was found to be only 59.8% +/- 32.6% (P < 0.01). The low bioavailability of the latter formulation was attributed to poor release of roxithromycin in the gastric site, which was proposed as a key factor to influence drug absorption. Other related factors were also discussed.

Adult↗

PubMed1998

[Synthesis and application of novel acrylic resin as enteric coating].

The pH sensitive two- and three-component acrylic resins were synthesized by radical solution copolymerization of methyl methacrylate (MMA), methacrylic acid (MAA) and/or butyl acrylate (BA) and their acid values were measured by acid-base titration. The dissolution of naproxen pellets coated with the synthesized resins in dissolution medium of different pH value was studied. The results show that the acrylic resin with different acid value can be prepared by adjusting the monomer ratios (MMA:MAA or MMA:MAA:BA). The smaller the acid value of the resin is, the higher pH sensitive value it has. The release of naproxen from pellets coated with these resins is greatly influenced by the pH value of the dissolution medium and the pH sensitive value of the coating resin. The three-component resins are plastic and can be used as coating material without adding plastisizers.

Acrylic Resins↗

PubMed1998

Common fragile sites and cancer (review).

Chromosomal fragile sites are specific loci which are especially susceptible to forming gaps, breaks and rearrangements in metaphase chromosomes when cells are cultured under conditions that inhibit DNA replication. Fragile sites are grouped into two classes the 'rare' and the 'common' fragile sites, based on their frequency of occurrence and means of induction. The common fragile sites are apparently present as a constant feature in all individuals and their clinical significance is that they might predispose chromosomes to breakage and rearrangement during cancer development. The most frequently observed common fragile sites occur, in decreasing order, at 3p14.2 (FRA3B), 16q23 (FRA16D), 6q26 (FRA6E), 7q32 (FRA7H), and Xp22 (FRAXB). FRA3B has been of particular interest since it is the most active common fragile site, and is located in a chromosomal band that is frequently deleted in several solid tumors suggesting that a putative tumor suppressor gene resides there. In this review we describe our work on the characterization of FRA3B and the analysis of deletions in the FRA3B region in several different tumor-derived cell lines. We also describe our efforts to identify other common fragile sites and to determine the role that these sites play in tumor development.

Acid Anhydride Hydrolases↗

PubMed1998

Pathogenesis of porcine Actinobacillus pleuropneumonia: Part I. Effects of surface components of Actinobacillus pleuropneumoniae in vitro and in vivo.

To understand the role of non-secreted components of Actinobacillus pleuropneumoniae in virulence, we investigated in vitro cytotoxicity and in vivo pulmonary changes in pigs due to various A. pleuropneumoniae (serotype 1) fractions. Following 1.5 h incubation, lipopolysaccharide (LPS), 2 crude extracts and bacterial culture supernatant (BCS) at high concentrations were cytotoxic to porcine pulmonary alveolar macrophages (PAM), peripheral blood mononuclear leucocytes, neutrophils and a cultured porcine bone marrow cell line. Heat-killed bacteria were cytotoxic to PAM after 24 h incubation. The 2 crude extracts were prepared by shaking either intact bacteria after removing culture supernatants (crude surface extract, CSE), or whole bacterial culture (crude surface plus culture supernatant extract, CSSE) with glass beads in saline at 60 degrees C. Further experiments showed that proteins from the bacterial membrane were partially involved in cytotoxicities of these 2 extracts. Both BCS and CSSE caused multivocal hemorrhage and neutrophil infiltration when inoculated into porcine lungs, but CSE did not. The lung:whole body weight ratios of the pigs treated with CSSE were significantly higher (P < 0.05) than those of pigs treated with BCS, CSE, or control solution. It is concluded that beside the secreted proteins, bacterial surface components including LPS and non-secreted proteins were cytotoxic in vitro; and secreted and non-secreted components act synergistically to cause lung lesions.

Actinobacillus Infections↗

PubMed1998

Evolution of a knowledge base for a clinical decision support system encoded in the Arden Syntax.

Clinical decision support systems (CDSS) are being used increasingly in medical practice. Thus, long-term maintenance of the knowledge bases (KB) of such systems becomes important. To quantify changes that occur as a KB evolves, we studied the KB at the Columbia-Presbyterian Medical Center. This KB has a total of 229 Medical Logic Modules (MLMs) encoded in the Arden Syntax. Eliminating those never used in practice, we retrospectively analyzed 156 MLMs developed over 78 months. We noted 2020 distinct versions of these MLMs that included 5528 changed statements over time. These changes occurred primarily in the logic slot (38.7% of all changes), the action slot (17.8%), in queries (15.0%) and in the data slot exclusive of queries (12.4%). We conclude that long-term maintenance of a KB for a CDSS requires significant changes over time. We discuss the implications of these results for the design of KB editors for the Arden Syntax.

Artificial Intelligence↗

PubMed1997

Regulatory cells generated by testicular tolerization to retinal S-antigen: possible involvement of IL-4, IL-10, and TGF-beta in the suppression of experimental autoimmune uveoretinitis.

Intratesticular injection of a retinal protein (S-antigen) into Lewis rats induces systemic immunotolerance (designated orchidic tolerance) and renders animals refractory to experimental autoimmune uveoretinitis (EAU) produced by S-antigen immunization. We demonstrated in this work that the immunotolerance could be transferred to syngeneic naive rats by both CD4+ and CD8+ regulatory cells. Attempts were then made to characterize the cytokines involved in the immunosuppressive activity of these regulatory cells. Using the in vitro lymphoproliferation assay, the inhibitory effect of CD4+ cells on effector cells was found to be reversed by antibodies against IL-4 and IL-10 but not by anti-TGF-beta antibody. IL-4 (IC50 = 1.6 ng/10(6) cells) and IL-10 (IC50 = 0.6 ng/10(6) cells) added to the assay medium were potent inhibitors of effector cell proliferation. Increased immunoreactivity and mRNA expression for IL-4 and IL-10 was observed for CD4+ regulatory cells. The inhibitory effect of CD8+ regulatory cells was reversed by anti-TGF-beta antibody but not by antibodies against IL-4 and IL-10. Compared with control CD8+ cells, CD8+ cells from tolerized rats demonstrated higher immunoreactivity for TGF-beta but did not show an enhanced expression of mRNA for TGF-beta. TGF-beta 1 and TGF-beta 2 added to effector cells showed dichotomous effects; both isoforms stimulated cell proliferation at 2.5 ng/10(6) cells and inhibited at lower or higher concentrations. These results led us to conclude that IL-4 and IL-10 are important cytokines for the immunosuppressive effect of CD4+ regulatory cells generated in orchidic tolerance. TGF-beta is an important immunosuppressive cytokine for CD8+ regulatory cells but further studies will determine whether other cytokines are also involved.

Animals↗

PubMed1997

IL-4 and IL-13 production in differentiated T helper type 2 cells is not IL-4 dependent.

CD4+ T cell differentiation into cells capable of producing IL-4 and IL-13 (Th2 cells) requires the presence of IL-4 and is STAT-6 dependent. Here we show that IL-4 is not required for IL-4 or IL-13 production by Th2 cells. Anti-IL-4 or anti-IL-4R Ab did not diminish IL-4 production by Th2 cells in response to TCR-mediated stimulation, nor did IL-4 enhance IL-4 production in response to stimulation of Th2 cells with limiting amounts of Ag. Th2 cells prepared from IL-4 knockout mice were capable of producing IL-13 mRNA in response to stimulation with immobilized anti-CD3. IL-4 did not increase IL-13 mRNA expression. Despite the failure of IL-4 to effect IL-4 production by primed Th2 cells, a STAT-6 binding element was demonstrated in the IL-4 promoter. The authenticity of this element was demonstrated by oligonucleotide competition, by supershifting with anti-STAT-6 Ab, and by IL-4-inducible effects on transcription of a reporter gene under the control of a multimerized element fused to an IL-4 minimal promoter. Nonetheless, an IL-4 promoter construct lacking the STAT-6 binding element was as effective as a construct containing this element in anti-CD3-induced reporter transcription. Thus, this element, if biologically active, must function at a step in T cell responsiveness distinct from the acute production of IL-4 by Th2 cells in response to Ag or anti-CD3.

Animals↗

PubMed1997

The NR2B-specific interactions of polyamines and protons with the N-methyl-D-aspartate receptor.

Many compounds exhibit NR2B-specific modulation of the N-methyl-D-aspartate receptor, although their mechanism(s) of action are largely unknown. Using chimeric NR2A/NR2B subunits, we have located a region of NR2B (amino acids 138-238) which regulated glycine-independent polyamine stimulation. Mutation of glutamate 201 in this region affected stimulation by polyamines in the order E201D < E201A < E201N < E201R. The relief of proton inhibition of the N-methyl-D-aspartate-induced currents mediated by these mutant receptors correlated with the reduction in glycine-independent polyamine stimulation. Electrophysiological evidence with a triple mutant of NR2A further supports the hypothesis that polyamine stimulation may be linked to the relief of tonic inhibition by protons and demonstrates the crucial role of amino acids 200 and 201 in polyamine stimulation. Polyamines and protons, therefore, share common NR2B determinants.

Amino Acid Sequence↗

PubMed1997

Glutathione peroxidase and catalase modulate the genotoxicity of arsenite.

The X-ray hypersensitive Chinese hamster ovary (CHO) cells, xrs-5, are also more sensitive to sodium arsenite in terms of cell growth and micronucleus induction than CHO-K1 cells. Since reactive oxygen species are suggested to be involved in arsenic toxicity, we have measured antioxidant mechanisms in xrs-5 as well as CHO-K1 cells. There were no apparent differences in the activities of superoxide dismutase, glutathione S-transferase, glutathione reductase, and the levels of glutathione between xrs-5 and CHO-K1 cells. However, the activities of glutathione peroxidase and catalase were 5.4- and 5.8-fold lower, respectively, in xrs-5 cells. The addition of catalase or glutathione peroxidase to cultures reduced the arsenite-induced micronuclei in xrs-5 cells. Whereas, simultaneous treatment with mercaptosuccinate, an inhibitor of glutathione peroxidase, and 3-aminotriazole, an inhibitor of catalase, synergistically increased the arsenite-induced micronuclei. These results suggest that both catalase and glutathione peroxidase are involved in defense against arsenite genotoxicity. The xrs-6 cells, another line of x-ray hypersensitive CHO cells, which had 1.6-fold higher catalase activity and 2.5-fold higher glutathione peroxidase activity than xrs-5 cells, were also more sensitive than CHO-K1 cells but were less sensitive than xrs-5 cells to cell growth inhibition of arsenite. Moreover, a 1.6-fold increase of glutathione peroxidase activity by selenite adaptation effectively removed the arsenite-induced micronuclei in CHO-K1 cells. These results suggest that glutathione peroxidase is more important than catalase in defending against arsenite toxicity. Our results also suggest that increasing the intracellular antioxidant level may have preventive or therapeutic effects in arsenic poisoning.

Amitrole↗

PubMed1997

Selective inhibition of neuronal nitric oxide synthase by N omega-nitroarginine-and phenylalanine-containing dipeptides and dipeptide esters.

A series of N omega-nitroarginine (ArgNO2)- and phenylalanine-containing dipeptides and dipeptide esters were synthesized as potential selective inhibitors of neuronal nitric oxide synthase (nNOS). All of the dipeptides and dipeptide esters are competitive inhibitors of nNOS, macrophage nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS), except for the ones that contain D-ArgNO2 (8-10, 12, 13), which are uncompetitive inhibitors of iNOS but competitive inhibitors of nNOS and eNOS. None of the dipeptides or dipeptide esters tested (1, 2, 12, 13) exhibited time-dependent inhibition of any of the NOS isoforms, unlike N omega-nitro-L-arginine itself, which does, although it is reversible. The order of the amino acids in the dipeptide or dipeptide ester is important to selectivity, and the selectivity depends on the chirality of the amino acids. In the case of the corresponding benzyl esters (5 vs 6), both dipeptides favor iNOS over nNOS and eNOS inhibition. All of the dipeptide methyl esters containing a D-amino acid, however, exhibit an inhibitory preference for nNOS over iNOS and eNOS. The most impressive selectivities observed are 1800- and 800-fold for 12 and 13, respectively, in favor of nNOS over iNOS; unfortunately, the selectivities of these compounds for nNOS over eNOS are only 2.5 and 5.3, respectively.

Animals↗

PubMed1997

Proteolytic activity of the ATP-dependent protease HslVU can be uncoupled from ATP hydrolysis.

HslVU is a new Escherichia coli ATP-dependent protease composed of two multimeric complexes: the HslU ATPase and the HslV peptidase. Prior studies indicated that HslVU requires ATP hydrolysis for the cleavage of peptides and proteins. We show here that ATP concentrations that activate hydrolysis of benzyloxycarbonyl-Gly-Gly-Leu-7-amido-4-methylcoumarin are 50-100 fold lower than those necessary for degradation of proteins (e.g. casein). Also, the nonhydrolyzable analogs of ATP, 5'-adenylyl beta, gamma-imidodiphosphate (AMP-PNP) and adenosine 5'-(alpha, beta-methylene)triphosphate, can support peptide hydrolysis, but only after an initial time lag not seen with ATP. This delay decreased at higher temperatures and with higher HslU or HslV concentrations and was eliminated by preincubation of HslU and HslV together. Thus, ATP hydrolysis accelerates the association of HslU and HslV, which occurs slowly with the nonhydrolyzable analog. The addition of KCl stimulated 4-6-fold the peptidase activity with AMP-PNP present and eliminated the time lag, but KCl had no stimulatory effect with ATP. NH4+ and Cs+ had similar effects as K+, but Na+ and Li+ were ineffective. AMP-PNP by itself supported hydrolysis of casein and other polypeptides only 20% as well as ATP, but in the presence of K+, Cs+, or NH4+, AMP-PNP activated casein degradation even better than ATP, although it was not hydrolyzed. In addition, MgCl2, MnCl2, and CaCl2 allowed some peptidase and caseinase activity in the absence of any nucleotide. However, Mn2+ and Ca2+, unlike Mg2+, abolished ATP hydrolysis and prevented further activation by ATP or AMP-PNP. These findings indicate that ATP binding to a high affinity site triggers the formation of an active state capable of peptide cleavage, although ATP hydrolysis facilitates this process. Rapid degradation of proteins requires a distinct state of the enzyme, which is normally reached through ATP hydrolysis at low affinity sites. However, AMP-PNP binding together with K+ can induce a form of HslVU that degrades proteins without energy consumption.

ATP-Dependent Proteases↗

PubMed1997

Activities and response to DNA damage of latent and active sequence-specific DNA binding forms of mouse p53.

The mouse p53 protein generated by alternative splicing (p53as) has amino acid substitutions at its C terminus that result in constitutively active sequence-specific DNA binding (active form), whereas p53 protein itself binds inefficiently (latent form) unless activated by C-terminal modification. Exogenous p53as expression activated transcription of reporter plasmids containing p53 binding sequences and inhibited growth of mouse and human cells lacking functional endogenous p53. Inducible p53as in stably transfected p53 null fibroblasts increased p21(WAF1/Cip-1/Sdi) and decreased bcl-2 protein steady-state levels. Endogenous p53as and p53 proteins differed in response to cellular DNA damage. p53 protein was induced transiently in normal keratinocytes and fibroblasts whereas p53as protein accumulation was sustained in parallel with induction of p21(WAF1/Cip-1/Sdi) protein and mRNA, in support of p53as transcriptional activity. Endogenous p53 and p53as proteins in epidermal tumor cells responded to DNA damage with different kinetics of nuclear accumulation and efficiencies of binding to a p53 consensus DNA sequence. A model is proposed in which C-terminally distinct p53 protein forms specialize in functions, with latent p53 forms primarily for rapid non-sequence-specific binding to sites of DNA damage and active p53 forms for sustained regulation of transcription and growth.

Animals↗

PubMed1997

The mechanism of inactivation of human placental S-adenosylhomocysteine hydrolase by (E)-4',5'-didehydro-5'-methoxyadenosine and adenosine 5'-carboxaldehyde oxime.

The mechanisms by which (E)-4',5'-didehydro-5'-methoxyadenosine (DMOA) and adenosine 5'-carboxaldehyde oxime (ACAO) inactivate S-adenosylhomocysteine (AdoHcy) hydrolase were elucidated in this study. Their inhibitory activities toward AdoHcy hydrolase were found to be time- and concentration-dependent, and DMOA and ACAO had K(i) and k2 values of 3.0 microM and 0.10 min(-1) and 0.67 microM and 0.16 min(-1), respectively. The inactivation of AdoHcy hydrolase by DMOA (and ACAO) occurs concomitantly with the reduction of the enzyme-bound NAD+ to NADH. The rates of enzyme inactivation correspond to the rates of NADH formation. Incubation of both DMOA and ACAO with the NAD+ form of AdoHcy hydrolase resulted in formation of 3'-ketoadenosine (3'-keto-Ado) 5'-carboxaldehyde and its 4'-epimer. Incubation of DMOA and ACAO with the apo form of the enzyme afforded adenosine (Ado) 5'-carboxaldehyde and its 4'-epimer. These results show that DMOA and ACAO are "proinhibitors" of the enzyme. They are first converted to the inhibitors (Ado 5'-carboxaldehyde and its 4'-epimer) in the active site of the enzyme; these inhibitors then inactivate the enzyme by a type I mechanism. The results from this study demonstrated that this is a common mechanism by which 4',5'-didehydroadenosine analogs, serving as substrates of both the 5'-hydrolytic activity and the 3'-oxidative activity of the enzyme, inactivate AdoHcy hydrolase. The results also provide further evidence supporting the hypothesis that AdoHcy hydrolase possesses a 5'-hydrolytic activity independent of the 3'-oxidation activity.

Adenosine↗

PubMed1997

NK1.1+ CD4+ T cells lose NK1.1 expression upon in vitro activation.

NK1.1+ CD4+ T cells produce IL-4 promptly in vivo upon injection of anti-CD3 and may play a role in initiating Th2 cell-mediated immunity. To characterize their in vitro activation properties, NK1.1+ CD4+ T cells were obtained in high purity from spleens of normal C57BL/6 mice, where they represent 2 to 5% of CD4+ T cells, or from MHC-class II I-Ab gene knockout mice, where they constitute 42% of CD4+ T cells. Activation of NK1.1+ CD4+ T cells from either source with plate-bound anti-CD3 resulted in loss of expression of NK1.1 as determined both by flow cytometric analysis and by reverse transcriptase-PCR analysis. A portion of these cells also lost CD4 expression. Both the CD4+ and CD4- activated cells retained the over-representation of V beta8 and V alpha14 chains and expressed the intermediate levels of the TCR-CD3 complex that is characteristic of resting NK1.1+ CD4+ T cells. The anti-NK1.1 mAb used for cell sorting was not the cause of NK1.1 or CD4 disappearance, since the sorted cells remain both NK1.1+ and CD4+ when cultured in the absence of anti-CD3 or in the presence of anti-CD3 and cyclosporin A. Furthermore, NK1.1+ CD4+ T cells that were not treated with anti-NK1.1 Ab also lost NK1.1 expression after activation. Populations of activated CD4+ and CD4- cells (derived from NK1.1+ CD4+ T cells) produced both IL-4 and IFN-gamma upon restimulation with plate-bound anti-CD3.

Animals↗

PubMed1997

The G protein alpha subunit (GP alpha1) is associated with the ER and the plasma membrane in meristematic cells of Arabidopsis and cauliflower.

Towards the elucidation of the cellular function(s) of GP alpha1, we have characterized its subcellular localization using immunofluorescence and cell fractionation. GP alpha1 is not present in nuclei or chloroplasts. It is a membrane-bound protein, and analysis of isolated endoplasmic and plasma membranes indicates a good correlation between GP alpha1 in both the plasma membrane and the ER compartment. Interestingly, these results may suggest more different functions for GP alpha1: it might be involved in transmission of extracellular signals across the plasma membrane and in the cytoplasm, and/or it may also be involved in regulating some aspects of the ER functions or membrane trafficking between both membranes.

Arabidopsis↗

PubMed1997

In differentiated CD4+ T cells, interleukin 4 production is cytokine-autonomous, whereas interferon gamma production is cytokine-dependent.

CD4+ T cells from T cell receptor transgenic mice that have been vigorously primed to be interleukin (IL)-4 producers (T(H2) cells) are capable of producing IL-4 even if restimulated in the absence of IL-4 and in the presence of IL-12. T cells vigorously primed in the absence of IL-4 (T(H1) cells) fail to produce IL-4 even if restimulated under conditions that would cause a naive T cell to produce IL-4. In contrast, interferon gamma (IFN-gamma) production is highly cytokine-regulated. T cells primed in the presence of IL-4 develop into IFN-gamma producers if IFN-gamma is included in the priming culture and if the cells are challenged in the presence of IL-12, presumably reflecting the role of IFN-gamma in inducing responsiveness to IL-12. Cells primed in the absence of IL-4 become highly responsive to IL-12 if IFN-gamma is included in the priming culture, and these cells are excellent IFN-gamma producers upon challenge; IL-12 considerably enhances their production of IFN-gamma. If cells are primed in the absence of IL-4 and IFN-gamma, they show very weak responsiveness to IL-12 as determined by STAT-4 activation. However, these cells acquire IL-12 responsiveness if cultured with IFN-gamma for a period as short as 4 hr. Thereafter, they produce large amounts of IFN-gamma upon challenge with antigen in the presence of IL-12. These results indicate that in primed CD4+ T cells, IL-4 production is largely cytokine-autonomous, whereas IFN-gamma production is highly cytokine-regulated.

Animals↗

PubMed1997

Involvement of calcium-dependent protein kinase C in arsenite-induced genotoxicity in Chinese hamster ovary cells.

Arsenic is the first metal to be identified as a human carcinogen. Arsenite, one inorganic form of arsenic, has been found to induce sister chromatid exchange, chromosome aberrations, and gene amplification in a variety of in vitro systems. In this study of arsenite-induced genotoxicity represented a micronuclei production in Chinese hamster ovary cells (CHO-K1), we found that the calcium channel blocker, verapamil, can potentiate arsenite-induced micronuclei. And after arsenite treatment, the elevation of intracellular calcium was observed. When extracellular calcium was depleted during arsenite treatment, the arsenite-induced micronuclei formation was significantly suppressed. These data indicated that a calcium ion plays an essential role in arsenite-induced genotoxicity. Further, it was found that the cotreatment of arsenite and a calcium ionophore, A23187, can increase the micronuclei induction. In contrast, pretreatment of the intracellular calcium chelator, quin 2, significantly inhibited micronuclei production of arsenite administration. In addition, we measured the activity of calcium- and phospholipid-dependent protein kinase C (PKC) and found that arsenite can activate PKC activity in a dose-dependent manner. Subsequently, some PKC activators and inhibitors were applied to investigate the involvement of PKC on arsenite-induced micronuclei formation. It was found that H7, a PKC inhibitor, can depress but TPA, a PKC activator, can enhance arsenite-induced micronuclei significantly. These data indicated that arsenite exposure perturbs intracellular calcium homeostasis and activates PKC activity. As a result, the activation of PKC activity may play an important role in arsenite-induced genotoxicity.

Adenosine Triphosphate↗