Disease relevance of MMS

• A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5alpha strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent [1].
• We delineated the clinical and laboratory features that help distinguish acute myelopathic MS (MMS) from acute transverse myelitis (ATM), specifically testing the hypothesis that the symmetry of motor and sensory impairments at presentation can reliably distinguish between ATM and MMS [2].
• The AtRecQsim gene suppressed the MMS hypersensitivity phenotype of the sgs1 cells [3].
• This method was used to quantify the levels of dTp(Me)dT in enzymatic hydrolysates of DNA obtained from a series of incubations of salmon testis DNA or mouse lymphoma cells with either MNU or MMS [4].
• These strains were slightly more resistant to the toxic effect of MMS and showed a reduced frequency of MMS-induced chromosomal aberrations [5].

Psychiatry related information on MMS

• In a double-blind, placebo-controlled study on the therapeutic efficacy and central effects of nicergoline, an ergot alkaloid with metabolic, antithrombotic and vasoactive action, 112 patients with mild to moderate dementia, diagnosed according to DSM III-R criteria (MMS 13-25), living in pensioners' homes, were included [6].
• If the MMS score is 23 or less, a set of criteria will be used to establish the diagnosis of vascular dementia [7].
• In this study we investigated the effects of the oral administration of citicoline alone (C1000:1000 mg/day; C500:500 mg/day) or in combination with nimodipine (C +NI:300 + 90 mg/day) during 4 weeks on memory performance in elderly subjects with memory deficits and without dementia (N = 24; age = 66.12 +/- 10.78 years; MMS score = 31.69 +/- 2.76) [8].
• The usefulness, inter-rater reliability, and validity of six mental tests, the MMS, the GMS, the MSQ, the VRT, the OLT, and the DCT were studied in 81 patients over the age of 75 years [9].

High impact information on MMS

• The GADD45-like genes are induced by environmental stresses, including MMS, UV, and gamma irradiation [10].
• Methyl methanesulfonate (MMS; 0.5 mM, 1 h) induced the same frequency of single strand breaks (SSBs) (2.1-2.3 X 10(-8) SSBs per dalton) in NHSF6 normal human and C3H 10T1/2 mouse cells [11].
• The effects of MMS on the expression of both gadd genes were inhibited by actinomycin D, suggesting that transcription is necessary for acute gadd induction.(ABSTRACT TRUNCATED AT 250 WORDS)[12]
• For the MMS, the cranial nerves concerned are V2, V3 and VII [13].
• Three systems play a role in the vascularization of cranial nerves: the inferolateral trunk (ILT), most often arising from the internal carotid artery, the middle meningeal system (MMS), and the ascending pharyngeal system (APS); the latter two are both derived from the external carotid artery [13].

Chemical compound and disease context of MMS

• Published data on mutations induced by ionizing radiation and 6 monofunctional alkylating agents, namely EMS, MMS, ENNG, MNNG, ENU and MNU, in different cell lines (Chinese hamster ovary, Chinese hamster lung V79, mouse lymphoma L5178 and human cells) were analysed so that radiation-equivalent chemical (REC) values could be calculated [14].
• Thirty-three patients with mild primary degenerative dementia according to DSM-III (MMS between 15 and 27) took part in a double-blind cross-over study of phosphatidylserine (Fidia, 300 mg/d) versus placebo [15].
• Mouse lymphoma L5178Y cells were treated with dimethyl sulphoxide (DMSO) as a standard solvent or reference agents known to induce oxidative damage (gamma irradiation and potassium bromate) or alkylation (methyl methanesulfonate, MMS; ethylnitrosourea, ENU) [16].
• The purpose of this study is to examine the accuracy of a 3D simulation generated by inclusion of various intensity-selected portions of spiral CT data into a proprietary software program (Preview, Medical Media Systems, MMS) in preoperative and postoperative assessment of the anatomical features of abdominal aortic aneurysm (AAA) [17].
• The 68,000 D MMS is a potent secretagogue and may play an important role in the regulation of mucus secretion, especially in chronic bronchitis and steroid-dependent asthma [18].

Biological context of MMS

• ScaANBS1 also participates in G2-M checkpoint control upon DNA damage caused by MMS [19].
• However, the accumulation of breaks in MMS-treated cellular DNA in the presence of novobiocin suggests that some "short-patch" alkylation repair may be inhibited by the antibiotic [20].
• 3-Aminobenzamide (3-AB) interferes with DNA repair and enhances lethality in growing MMS (methyl methane sulfonate)-treated human fibroblasts [21].
• Our results also show that, in contrast to C. elegans chk2, Drosophila chk2 is not essential for normal meiosis and recombination, and it also appears to be dispensable for the MMS-induced DNA damage checkpoint and the HU-induced DNA replication checkpoint during larval development [22].
• No effect of treatment with MMS, QM, and Q on the distribution of SCEs in chromosomes was found compared with controls [23].

Anatomical context of MMS

• The amount of AP sites in MMS-treated HeLa cells transiently increased at 3 h, then gradually decreased to 40% at 24 h [24].
• Patients assigned to the MMS group had onset of MS symptoms referable to the spinal cord and eventually fulfilled Poser's criteria for MS [2].
• However, transfectants derived from mutant cell line MMS-2 gained significant resistance to both N-methyl-N'-nitro-N-nitrosoguanidine and N-nitroso-N-methylurea, whilst retaining sensitivity to MMS [25].
• For the induction of diploid spermatids positive results were only obtained for MMS and parafluorophenylalanine [26].
• The possible existence of a threshold for compounds inducing chromosomal loss was investigated for four known aneugens (colchicine, COL; carbendazim, MBC; mebendazole, MEB; nocodazole, NOC) and two clastogens (methyl methanesulfonate, MMS; mitomycin C, MMC) using the micronucleus (MN) test in human lymphocytes [27].

Associations of MMS with chemical compounds

• Expression of the N169A and N169S AAG variants in S. cerevisiae during methyl methanesulfonate exposure resulted in greater sensitivity, greater mutation induction following MMS exposure, and more strand breaks in vivo [28].
• The presence of adenine, an inhibitor of AP endonucleases, in the repair incubation of MMS-treated cells induced moderate accumulation of AP sites, suggesting inhibition of the activities of MPG as well as AP endonucleases by adenine metabolites [24].
• Denbufylline induced a statistically significant and clinically relevant improvement in both SDAT and MID patients, whereas after placebo this was not the case in CGI, the TMT, and the DS, with interdrug differences being significant in all primary target variables such as the CGI, MMS, SCAG, and DSST [29].
• 3-Aminobenzamide is lethal to MMS-damaged human fibroblasts primarily during S phase [21].
• This effect was also seen when MNU pretreatment was used, but not with MMS or streptozotocin [30].

Regulatory relationships of MMS

• In the cells with the highest basal ADPRT activity 12 h after block release, the MMS-induced ADPRT stimulation could not be observed [31].

Other interactions of MMS

• This correlation was even better between PTH levels and MMS fr [32].
• Expression of hRAD50 partially rescued the MMS (methyl methanesulfonate)-sensitive phenotype in rad50 mutant yeast, whereas hRAD50-3 did not show complementation [33].
• Our data suggest a protective role for GM-CSF, IL-3 or other MMS cytokines in preventing SFI in patients receiving HDC [34].
• The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS [35].
• The lethality of 3-AB to a population of asynchronously cycling cells treated with MMS is thus the summation of effects on the cells as they traverse S phase [21].

Analytical, diagnostic and therapeutic context of MMS

• The ligation curve calibrated for such extra SSBs also revealed no delaying effect of 3AB on the rate of ligation of MMS-induced SSBs in 10T1/2 cells [11].
• This frequency was significantly increased after treatment with MMS [23].
• This approach is demonstrated with an immortalized lung cell culture (A549, human lung carcinoma epithelia) in response to a variety of inhalation hazards including gliotoxin (a fungal metabolite), etoposide (a genotoxin), and methyl methansesulfonate (MMS, an alkylating agent) [36].
• Herpes simplex virus type I (Strain KOS) is inactivated by treatment with MMS, MNNG and HN2 as determined by plaque assay on Vero cell monolayers, or by an infectious center assay with FS2 cells, human foreskin fibroblast line [37].
• Because MMS is usually performed with local anesthesia on an outpatient basis, it is cost effective, safe, and extends operability to patients who are poor candidates for general anesthesia [38].

References