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G Los

Publications and source records attributed to G Los.

58 records · Page 4Linked to original sources
PubMed1987

The absence of delayed-type hypersensitivity reactivity in a syngeneic murine tumour system.

In different murine systems, delayed-type hypersensitivity (DTH) swelling responses at 24-48 hr after antigen challenge were preceded by an early 2-hr swelling response. The 24-hr DTH response is thought to depend on this early (DTH-initiating) hypersensitivity response. In this paper we show that in the syngeneic DBA/2-SL2 murine tumour system only an early 2-hr swelling response can be evoked. This early hypersensitivity response was tumour specific and serotonin dependent. The early hypersensitivity response in contact hypersensitivity has been ascribed to antigen-specific T-cell factors. To test whether similar T-cell factors were involved in the early hypersensitivity response in this syngeneic tumour system, we have transferred lymph node, spleen lymphocytes and serum from immunized mice into naive recipients. The serum was fractionated in two fractions, a 50,000-80,000 MW fraction, and a 120,000-190,000 MW fraction. In recipients of lymphocytes, total serum and the 50,000-80,000 MW fraction of the serum, an early hypersensitivity response can be evoked. So, these data suggest the involvement of specific T-cell factors in the development of an early hypersensitivity response against syngeneic tumour cells. Despite the development of an early (DTH initiating) hypersensitivity swelling response these immunized animals cannot develop a classical 24-hr swelling response. This absence of the 24-hr response in the presence of the 2-hr response is discussed in relation to the frequently observed immune suppression in tumour-bearing mice.

Animals↗
PubMed1986

In vivo 31P-nuclear magnetic resonance study of the response of a murine mammary tumor to different doses of gamma-radiation.

The response of the s.c. implanted murine mammary carcinoma NU-82 to 10 and 20 Gy of gamma-radiation was followed by in vivo 31P-nuclear magnetic resonance spectroscopy on 48 mice during a period of 2 days. During the first 8 h after a dose of 10 Gy, the ratio of ATP/inorganic phosphate increases to a value of 120 +/- 15% (SE) of the control value. This rise is followed by a decrease of the ratio to 74 +/- 12% after 47 h. However treatment with 20 Gy causes the ratio of ATP/Pi to decrease gradually to a level of 45 +/- 7% after 47 h. Histological investigations demonstrated that radiation-induced necrosis largely contributes to this phenomenon. During the time of observation irradiated tumors displayed no changes in size and intracellular pH. After treatment with 10 Gy as well as with 20 Gy, the phosphodiester resonance decreased in intensity. By 31P-nuclear magnetic resonance spectroscopy on extracts of the NU-82 tumor, two phosphodiesters were identified, glycerophosphocholine and glycerophosphoethanolamine.

Adenosine Triphosphate↗
PubMedDate not supplied

Reduction of cisplatin nephrotoxicity by sodium selenite. Lack of interaction at the pharmacokinetic level of both compounds.

Administration of sodium selenite (Na2SeO3) 1 hr before cis-diamminedichloroplatinum(II) (referred to herein as cisplatin) can protect against the nephrotoxicity of cisplatin. The pharmacokinetic aspects of this interaction were studied in rodents with radiolabeled selenite and cisplatin. Total [75Se]selenium in plasma consisted of [75Se] selenium in plasma proteins and [75Se]selenite in plasma ultrafiltrate. After a short distribution phase, the elimination of [75Se]selenite and total [75Se]selenium proceeded biphasically in the rat, with an initial plasma elimination half-life of [75Se]selenite of 22 +/- 2 min. Coadministration of cisplatin had no effect on the initial nor on the much slower terminal elimination phase of [75Se]selenite nor of total [75Se] selenium. Sodium selenite, in doses protecting against the nephrotoxicity of cisplatin, did not significantly affect areas under the plasma concentration time curve from 0-6 hr nor the initial plasma half-lives of [195mPt]cisplatin (t1/2, 28 +/- 2 min) and total [195mPt]platinum (t1/2, 30 +/- 3 min) in plasma. The much slower terminal elimination phases in plasma and the cumulative urinary excretion of [195mPt] cisplatin and total [195mPt]platinum were neither influenced by sodium selenite. Sodium selenite does not react chemically with cisplatin in vitro. Apparently, bioactivation of selenite is required for its protective effect in vivo. Distribution studies in a mice tumor model indicated that [75Se]selenium is concentrated strongly in the kidney and that the bioactivation of selenite also most likely occurs primarily in the kidneys. We conclude that sodium selenite protects rodents against cisplatin-induced nephrotoxicity without influencing the systemic availability of cisplatin and total platinum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗