Cataracts Produced in Rats by 1,4-Dimethanesulfonoxybutane (Myleran)

Solomon, Cyril; Light, Albert; Beer, Edwin

doi:10.1001/archopht.1955.00930020856006

Cited by 21 publications

(3 citation statements)

References 9 publications

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“…One BU‐treated mouse autopsied at day 127 was found to have a unilateral cataract, but on histological examination, no other lesions were found to be present in the eye. BU is known to be a potent cataractogenic agent (Solomon et al . 1955; Grimes et al .…”

Section: Discussionmentioning

confidence: 99%

Further development of a model of chronic bone marrow aplasia in the busulphan‐treated mouse

Turton

Sones

Andrews

et al. 2006

Int J Experimental Path

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Aplastic anaemia (AA) in man is an often fatal disease characterized by pancytopenia of the peripheral blood and aplasia of the bone marrow. AA is a toxic effect of many drugs and chemicals (e.g. chloramphenicol, azathioprine, phenylbutazone, gold salts, penicillamine and benzene). However, there are no widely used or convenient animal models of drug-induced AA. Recently, we reported a new model of chronic bone marrow aplasia (CBMA 5 AA) in the busulphan (BU)-treated mouse: eight doses of BU (10.50 mg/kg) were administered to female BALB/c mice over a period of 23 days; CBMA was evident at day 91/112 post-dosing with significantly reduced erythrocytes, platelets, leucocytes and nucleated bone marrow cell counts. However, mortality was high (49.3%). We have now carried out a study to modify the BU-dosing regime to induce CBMA without high mortality, and investigated the patterns of cellular responses in the blood and marrow in the post-dosing period. Mice (n 5 64/65) were dosed 10 times with BU at 0 (vehicle control), 8.25, 9.0 and 9.75 mg/kg over 21 days and autopsied at day 1, 23, 42, 71, 84, 106 and 127 post-dosing (n 5 7-15); blood and marrow samples were examined. BU induced a predictable bone marrow depression at day 1 post-dosing; at day 23/42 post-dosing, parameters were returning towards normal during a period of recovery. At day 71, 84, 106 and 127 post-dosing, a stabilized, late-stage, nondose-related CBMA was evident in BU-treated mice, with decreased erythrocytes, platelets and marrow cell counts, and increased MCV. At day 127 post-dosing, five BU-treated mice showed evidence of lymphoma. In this study, mortality was low, ranging from 3.1% (8.25 mg/kg BU) to 12.3% (9.75 mg/kg BU). It is concluded that BU at 9.0 mg/kg (or 9.25 mg/kg) is an appropriate dose level to

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Section: Discussionmentioning

confidence: 99%

Further development of a model of chronic bone marrow aplasia in the busulphan‐treated mouse

Turton

Sones

Andrews

et al. 2006

Int J Experimental Path

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“…The relative effec¬ tiveness of this agent is indicated in the over-all similarity of its effects to those in¬ duced by 500-600 rads of x-radiation (85-95 rads/min) or 280 rads of -.0 mev fast neutrons (100 rads/min). Although 4M20-induced cataracts were similar in severity to those induced by radiation, this quinoline compound is significantly more cataracto¬ genic than the "radiomimetic" agent busulfan (Myleran), which from studies on rats 4 and mice 1 appears, in turn, more cata¬ ractogenic than HN:2 or TEM at midlethal dose levels (Fig 1).…”

Section: Commentmentioning

confidence: 85%

Induction of Cataracts in Mice by 4-(p-Dimethylaminostyryl) Quinoline

Christenberry¹,

Conklin²,

Upton³

et al. 1963

Archives of Ophthalmology

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“…Large doses affect the cells of the lens and cause cataract, Solomon, Light andde Beer (1955, 1956). Histologically, von Sallmann (1 957) found nuclear fragmentation and pyknoses as well as atypical mitoses and later hydropic and vacuolized cytoplasms.…”

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confidence: 99%