Studies on Desoxyribonuclease in Systemic Lupus Erythematosus. Non-Participation of Serum Desoxyribonuclease in the “L.E. Phenomenon” 1

Kurnick, N. B.; Pariser, Sanford; Schwartz, Lawrence; Lee, Stanley L.; Irvine, Wallace

doi:10.1172/jci102696

Cited by 21 publications

(6 citation statements)

References 18 publications

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“…There was no evidence of L.E. cell transformation in these in vivo studies, thus corroborating the earlier in vitro work of Kurnick, Pariser, Schwartz, Lee, and Irvine (23).…”

Section: Clinical-pathological Laboratory Determinationssupporting

confidence: 89%

The Intravenous Injection of Bovine Crystalline Pancreatic Desoxyribonuclease into Patients1

Johnson¹,

Goger²,

Tillett³

1954

J. Clin. Invest.

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In connection with investigations of streptococcal desoxyribonuclease contained in Varidase@,2 comparative observations have included the intravenous administration of crystalline pancreatic desoxyribonuclease in patients (1).Crystalline pancreatic desoxyribonuclease (referred to throughout this article as PD) has been isolated from beef pancreas and its general properties determined (24). The crystalline material 8 made according to the methods of Kunitz, has been employed in this study.The results to be described center primarily around the intravenous injection of PD into patients. In addition, observations have been made on the renal excretion and clearance of PD, its diffusion into various extravascular areas and the effect of intrathecal injections in adults and children with and without meningitis. Extensive clinical and laboratory examinations have been made for evidence of toxicity.The categories of the studies may be listed as: a) Toxicity studies following intravenous and intrathecal injections; b) blood levels following intravenous infusions; c) "naturally" occurring inhibitor for PD (in the general circulation); d) renal excretion and clearance; e) diffusion into the peritoneal and pleural fluids, wound exudates, bronchial secretions and cerebro-spinal fluid; and f) the development of specific antibodies.A discussion of the potential therapeutic implications of PD follows. (DNA) was prepared by adding the dried sodium thymonucleate to M/40 veronal buffer pH 7.5, and agitating in a shaking machine until the DNA went into solution. After shaking, the solution was heated at 56°C. for 5 to 25 hours until residual depolymerase activity was destroyed. Further heating was used (a) to reduce the viscosity to a specific viscosity of about 5 to 7.0 (4.0 centipoise to 5.6 centipoise) and (b) to inhibit the "reactivity" of the DNA. Inasmuch as the assay value for a standard control solution of desoxyribonuclease could be decreased by prolonged heating of the DNA substrate used for its assay, it seemed likely that the "reactivity" of the DNA was controlled by this heating. This decrease occurred without an apparent change in the viscosity of the DNA. In order to obtain consistent and reproducible results with this enzyme assay, it proved to be obligatory to control these three variables: the stability, viscosity, and "reactivity" of the substrate. Mg++ was added to the DNA solution after heating to a final concentration of .003 M. Desoxyribonuclease assayThe assay for desoxyribonuclease activity (5) was modified as follows: a) 0.1 ml. or 0.2 ml. of sample was used interchangeably as required, for optimum enzyme concentration in the assay; b) recovery experiments with PD in neopeptone buffer, urine, and cerebro-spinal fluid indicated a linear relationship between enzyme concentration and decrease in viscosity of the DNA substrate from 0.2 to 0.8 viscosity units in 10 minutes. However, PD in inhibitor-free sera could not be measured accurately unless the reduction in viscosity was at least 0.4 viscosity units i...

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“…There was no evidence of L.E. cell transformation in these in vivo studies, thus corroborating the earlier in vitro work of Kurnick, Pariser, Schwartz, Lee, and Irvine (23).…”

Section: Clinical-pathological Laboratory Determinationssupporting

confidence: 89%

The Intravenous Injection of Bovine Crystalline Pancreatic Desoxyribonuclease into Patients1

Johnson¹,

Goger²,

Tillett³

1954

J. Clin. Invest.

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“…We suggest that the L.E. plasma factor (27), which itself has no DNase activity (5), causes the release of the intracellular DNase from inhibition. The inhibition of the "L.E.…”

Section: Discussionmentioning

confidence: 83%

“…cell" (2), we have suggested (3), as have Klemperer and his associates (4), that an increased serum enzyme activity, potentiation of an intracellular DNase, or destruction of an intracellular inhibitor of DNase by a serum factor, might be responsible. In a previous communication (5) we reported evidence which excludes the serum DNase from responsibility for the phenomenon. Studies on the interaction of leucocytes and serum, in an approach to the alternative possibilities, disclosed the presence of a specific intracellular inhibitor of human serum DNase and an inhibitor of the "L.E.…”

mentioning

confidence: 87%

“…phenomenon (a. classical "L.E. cell" with single large inclusion, or "droplet cell" with several small inclusions, b. rosettes, c. "globs" [5]) was graded from 0 to 4 on the basis of frequency of occurrence.…”

Section: "Le Cell" Phenomenon Inhibitormentioning

confidence: 99%

“…SERUM DNAsE INHIBITION A. Preparation of leucocyte extracts Leucocytes (WBC) were prepared with the aid of Bovine fraction I from heparinized blood as previously described (5) or by centrifugation at 0 to 2°C of fresh "ACD" bloods (120 ml. of 1.47 ml.…”

mentioning

confidence: 99%

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A Specific Inhibitor for Human Desoxyribonuclease and an Inhibitor of the Lupus Erythematosus Cell Phenomenon From Leucocytes 1

Kurnick¹,

Schwartz²,

Pariser³

et al. 1953

J. Clin. Invest.

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In speculating upon the probable role of desoxyribonuclease (DNase) in the depolymerization of desoxyribonucleic acid (DNA), which characterizes (1) the "lupus erythematosus (L.E.) cell" (2), we have suggested (3), as have Klemperer and his associates (4), that an increased serum enzyme activity, potentiation of an intracellular DNase, or destruction of an intracellular inhibitor of DNase by a serum factor, might be responsible. In a previous communication (5) we reported evidence which excludes the serum DNase from responsibility for the phenomenon. Studies on the interaction of leucocytes and serum, in an approach to the alternative possibilities, disclosed the presence of a specific intracellular inhibitor of human serum DNase and an inhibitor of the "L.E.cell" phenomenon (6, 7). In the present paper, we shall report upon some of the characteristics of these factors.

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The Relationship of Systemic Lupus Erythematosus and Discoid Lupus Erythematosus

SCOTT¹

1959

AMA Arch Derm

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Studies on Desoxyribonuclease in Systemic Lupus Erythematosus. Non-Participation of Serum Desoxyribonuclease in the “L.E. Phenomenon” 1

Cited by 21 publications

References 18 publications

The Intravenous Injection of Bovine Crystalline Pancreatic Desoxyribonuclease into Patients1

The Intravenous Injection of Bovine Crystalline Pancreatic Desoxyribonuclease into Patients1

A Specific Inhibitor for Human Desoxyribonuclease and an Inhibitor of the Lupus Erythematosus Cell Phenomenon From Leucocytes 1

The Relationship of Systemic Lupus Erythematosus and Discoid Lupus Erythematosus

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