Disease relevance of ARSANILIC ACID

• We have developed a new synthetic compound, ammonium tri-chloro(dioxoethylene-O,O'-)tellurate (AS-101), which has immunomodulating properties and minimal toxicity [1].
• In addition, AS-101 could directly enhance the ratio of OKT4 to OKT8-positive cells in cultured mononuclear cells from AIDS (acquired immune deficiency syndrome) patients [1].
• Murine monoclonal antibodies (Mabs) directed against Fisher Immunotype 1 Pseudomonas aeruginosa and a nonmicrobial, nonmammalian haptene, p-arsanilic acid, were labeled with 125I by the lodogen-Bead method [2].
• Mice of strain A/J responded to repeated intraperitoneal injection of Limulus hemocyanin derivatized with arsanilic acid by producing large quantities (approximately 5 mg/mL of ascites fluid) of IgG antibodies specific for this hapten [3].
• Inhibition of the reverse transcriptase activity and replication of human immunodeficiency virus type 1 by AS 101 in vitro [4].

Psychiatry related information on ARSANILIC ACID

• In a preparatory experiment, acute IDPN (890 mg/kg, IP) and intratympanic arsanilic acid caused similar alterations in locomotor activity, rearings, and scores for vestibular impairment [5].

High impact information on ARSANILIC ACID

• Splenocytes of BALB/c mice injected with AS-101 increased production of IL-2 and CSF in vitro in the presence of mitogen [1].
• Splenocytes of mice treated in vivo with AS-101 expressed high levels of IL-2 receptor [1].
• Mononuclear cells of normal donors acquired responsiveness to recombinant IL-2 and bound monoclonal antibody to IL-2 receptor after incubation with AS-101 [1].
• The stimulation of lymphocytes by AS-101 apparently involves an increase in intracellular free calcium [1].
• Painting mice on the skin with the diazonium salt of p-arsanilic acid elicited two types of T cell activity [6].

Chemical compound and disease context of ARSANILIC ACID

• The antitumor drug AS-101 [ammoniumtrichloro (dioxoethylene-O,O')tellurate(IV)] is the first tellurium-containing compound that has been identified as possessing immunomodulating properties and minimal toxicity [7].
• It also confirms that 3-nitro has a higher absolute toxicity than arsanilic acid in pigs as well as a lower margin of safety [8].

Biological context of ARSANILIC ACID

• An excess of births of heterozygotes in the offspring of the 107 AS mothers (144 AS:89 AA, chi2=12.98; p<0.001) and 95 AT mothers (117 AT:66 AA, chi2=14.21; p<0.001) married to homozygous normal fathers was observed, but not for births to the reverse parental combinations (103 AS: 101 AA, chi2=0.019; p=0.89 and 57 AT:42 AA, chi2=2.27; p=0.13) [9].
• The results confirm the mode of action of AS-101 as a real modulating agent of cell proliferation [10].
• Dietary salt (NaCl) levels (.2, .5%), dietary arsanilic acid levels (0, 100, 200 ppm), supplemental copper levels (0, 125, 250 ppm) and waste management systems (oxidation ditch, anaerobic deep pit, anaerobic lagoon) were compared in this series of studies [11].

Anatomical context of ARSANILIC ACID

• CRIA+ and CRIA+/- clonotypes were as heterogeneous as CRIA- antibodies, but a majority of CRIA+/- clones maintained a characteristic relative affinity for two of the haptens, p-arsanilic acid (p-ARS) and p-azobenene arsonic acid-N-tyrosine (ABA-tyr), which was identical to the prototype CRIA+ hybridoma protein R16 [12].
• A crude preparation of alkaline phosphatase (EC 3.1.3.1) from calf intestinal mucosa was purified by affinity chromatography on Sepharose-bound derivatives of arsanilic acid, which was found to be a competitive inhibitor of the enzyme [13].
• Although both AS-101 and interferon (IFN)-gamma inhibit IL-10, AS-101, unlike IFN-gamma, does not prime macrophages for LPS-induced nitric oxide release and does not appear to significantly affect monocyte HLA-DR expression [14].
• The immunomodulator AS-101 inhibits IL-10 release and augments TNF alpha and IL-1 alpha release by mouse and human mononuclear phagocytes [14].
• Results showed that dietary inclusion of 50 and 100 mg/kg of 4-arsanilic acid significantly improved feed utilization and egg production, but the concentration of As in the tissues and feces in groups fed 4-arsanilic acid was higher than in control group [15].

Associations of ARSANILIC ACID with other chemical compounds

• Complete recovery of pure aqueous solutions of As(III), As(V), cacodylic acid (DMA), monomethylarsinic acid (MMA), and o-arsanilic acid was attained by using both nickel and palladium modifiers [16].
• GSSG reductase catalyzed the oxidation of NADPH by p-arsanilic acid [17].
• In the present study we show that AS-101 selectively augments the release of TNF alpha and IL-1 alpha and inhibits the release of IL-10 by lipopolysaccharide (LPS)-stimulated mouse peritoneal macrophages and human monocytes [14].
• In the present study, arsanical-based affinity chromatography for pyruvate kinase (PK) isolation was explored. p-Arsanilic acid (4-aminophenyl arsonic acid), which contains an arsonic acid moiety structurally similar to inorganic pentavalent arsenate, was conjugated to Sepharose 4B via its para-amino group to form an As(V)-Sepharose matrix [18].

Gene context of ARSANILIC ACID

• In vivo treatment of Balb/c mice with AS-101 caused a significantly increased production of IL-2 and CSF in vitro in the presence of mitogen [19].
• AS-101 inhibited the production of IL-10, IFNgamma, IL-2R and IL-5 in both PAA patients and controls, but there was a greater inhibitory effect in children with PAA [20].
• Effect of the new immunoregulator AS-101 on in vitro functions of mononuclear cells from patients with systemic lupus erythematosus [21].
• The ability of AS-101 to potentiate the effects of chemotherapeutic drugs and augment cytokine production in vivo has led to clinical trials on AS-101 which are currently being carried out in cancer patients [14].

Analytical, diagnostic and therapeutic context of ARSANILIC ACID

• These results indicate that AS-101 is potentially useful in the treatment of clinical conditions involving immunosuppression [1].
• AS-101 was found to be non-toxic to cells from both patient and control groups; it increased the production of IL-2, elevated the percentage of Tac-positive cells even among cells that had been pre-treated with pronase, and ameliorated the absorption of IL-2 [21].
• Synthetic peptides containing these amino acids were modified with diazotized arsanilic acid and subjected to N-terminal sequence analysis [22].
• Fluorimetric determination of arsanilic acid by flow-injection analysis using on-line photo-oxidation [23].

References