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Biomedical subjects

M T Goldberg

Publications and source records attributed to M T Goldberg.

24 records · Page 2Linked to original sources
PubMed1983

Nuclear aberrations as a short-term test for genotoxicity to the colon: evaluation of nineteen agents in mice.

The genotoxicity of 16 agents including several hydrazines, nitrosamines, aromatic amines, polycyclic hydrocarbons, and other related compounds and three known inhibitors of carcinogenesis was assessed in the murine colonic nuclear aberration assay. Of the seven agents considered positive for colonic DNA damage, five were large bowel carcinogens. All structural analogues of the intestinal carcinogens that are tumorigenic for other organs, with the exception of benzo[a]pyrene, were negative in the colonic nuclear aberration assay as were all noncarcinogens tested. The metabolic inhibitor disulfiram completely inhibited 1,2-dimethylhydrazine-induced colonic nuclear damage, while inhibition was less marked for the antioxidants butylated hydroxyanisole and caffeic acid. The versatility of the assay as an indicator of colonic genotoxicity resulting from carcinogen exposure is discussed.

1,2-Dimethylhydrazine↗
PubMed1978

Elevated vascular reactivity in the timolol-treated spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) treated in utero with a low dose, and from weaning with 6 mg/kg per day of oral timolol, a noncardioselective beta-adrenergic blocker, did not develop hypertension. Isolated aortic rings from these animals showed increased reactivity to raised extracellular K+, when compared with tissues from timolol-treated Kyoto-Wistar (WKY) control rats. The normotensive SHR aorta also showed significant responsiveness to H+ and to high Ca2+ concentrations without previously depolarizing the tissue with high K+. These observations suggest that the increased reactivity seen in vascular smooth muscle from this animal does not develop secondary to elevated peripheral resistance and subsequent hypertrophy, and that the initiation of hypertension in this animal may be related to a membrane defect and (or) cellular defect which results in a facilitation of Ca2+ availability for the contractile proteins of the SHR vascular smooth muscle cell.

Animals↗
PubMed1977

An analysis of the action of lanthanum on aortic tissue from normotensive and spontaneously hypertensive rats.

Significant tension development resulting from the administration of lanthanum salts (La3+) to isolated aorta tissues was observed in preparations from the spontaneously hypertensive rat (SHR) but not in preparation from age-matched normotensive Wistar rats (NWR). The response to La3+ was significantly greater in tissues maintained in bicarbonate-buffered Krebs than observed in bicarbonate and phosphate-free HEPES-buffered Krebs. At least part of the LA3+ response in the bicarbonate- and phosphate-buffered solutions was due to a pH shift and could be mimicked by raising the extracellular hydrogen ion [H+] concentration. However, a direct action of La3+ on excitation-contraction coupling could be observed in HEPES-buffered solutions where the addition of La3+ also resulted in tension development but no significant pH change; this action of La3+ was found to be resistant to inhibition by maintenance in a Ca2+-free medium and (or) D-600 pretreatment suggesting an intracellular action for La3+. The paradoxical response to both H+ and La3+ in the SHR aorta suggests that the muscle membrane may be more permeable to these ions and, in addition, suggests that the membrane and (or) intracellular calcium stores in this tissue may also be more labile than those in the normotensive controls.

Animals↗