Endocrine control of extrathyroidal peroxidases and iodide metabolism

1985 ◽  
Vol 110 (3) ◽  
pp. 383-387 ◽  
Author(s):  
Swapan K. De ◽  
Chayan K. Ganguly ◽  
Tapan K. Chakraborty ◽  
Arya K. Bose ◽  
Ranajit K. Banerjee

Abstract. The role of the thyroid and adrenal glands on iodide transport and peroxidase-catalyzed formation of iodotyrosines in extrathyroidal tissues such as stomach and submaxillary glands has been investigated. Thyroidectomy stimulates iodide concentration and iodotyrosine formation in stomach, sensitive to the administration of thyroxine but having no effect on the peroxidase activity. In contrast, although thyroidectomy stimulates the submaxillary peroxidase which is reversed on treatment with thyroxine, it has no effect on iodide concentration and organification in the submaxillary gland. Gastric peroxidase activity is specifically stimulated by adrenalectomy and is inhibited by glucocorticoids which also inhibit iodotyrosine formation in stomach.

1983 ◽  
Vol 31 (6) ◽  
pp. 776-782 ◽  
Author(s):  
H Iwao ◽  
N Nakamura ◽  
F Ikemoto ◽  
K Yamamoto

The distribution of exogenously administered renin was investigated using whole body autoradiography. Purified renin from mouse submaxillary gland (SR) was labeled with radioactive iodine (125I). This labeled renin (125I-SR) and Na125I were administered into the tail vein of male ddY mice, in doses of 10.2 and 16.4 mu Ci/30 g body weight, respectively. Mice were killed by an overdose of ether, and autoradiography was performed on whole body sections. To separate free 125I liberated from 125I-SR, sections were treated with perchloric acid. A major accumulation of 125I-SR, acid-insoluble, was evident in the renal cortex, whereas the hepatic accumulation of 125I-SR was minor. Radioactivity in the thyroid and submaxillary glands, in the stomach, and in urine was also apparent, but disappeared after acid treatment, except in the thyroid glands. Radioactivity in the brain, intestinal content, spleen, and adrenal glands was nil. These autoradiograms provide the first evidence that exogenously administered renin is mainly distributed in the renal cortex.


1971 ◽  
Vol 58 (3) ◽  
pp. 340-350 ◽  
Author(s):  
G. L. Alonso ◽  
P. M. Bazerque ◽  
D. M. Arrigó ◽  
O. R. Tumilasci

Microsomes from rat submaxillary glands are able to take up calcium from the suspension media. Calcium uptake is greatly increased by the presence of ATP. This effect of ATP is not detected at 0°C. ADP cannot replace ATP to potentiate calcium uptake. ATP-dependent calcium uptake is not observed in the absence of magnesium. ATP-dependent calcium uptake is enhanced by oxalate and, to a lesser degree, by inorganic phosphate. Total calcium per milligram of microsomal protein observed when tests were performed without oxalate closely parallels the amounts for skeletal and cardiac muscles reported by several authors. Calcium uptake in salivary gland microsomes is slower than in muscle microsomes. Speculations are considered about the role of ATP-dependent calcium uptake. It is suggested that a decrease in intracellular free calcium levels returns these cells to the resting state after secretion.


1991 ◽  
Vol 56 (4) ◽  
pp. 923-932
Author(s):  
Jana Stejskalová ◽  
Pavel Stopka ◽  
Zdeněk Pavlíček

The ESR spectra of peroxidase systems of methaemoglobin-ascorbic acid-hydrogen peroxide and methaemoglobin-haptoglobin complex-ascorbic acid-hydrogen peroxide have been measured in the acetate buffer of pH 4.5. For the system with methaemoglobin an asymmetrical signal with g ~ 2 has been observed which is interpreted as the perpendicular region of anisotropic spectrum of superoxide radical. On the other hand, for the system with methaemoglobin-haptoglobin complex the observed signal with g ~ 2 is symmetrical and is interpreted as a signal of delocalized electron. After realization of three repeatedly induced peroxidase processes the ESR signal of the perpendicular part of anisotropic spectrum of superoxide radical is distinctly diminished, whereas the signal of delocalized electron remains practically unchanged. An amino acid analysis of methaemoglobin along with results of the ESR measurements make it possible to derive a hypothesis about the role of haptoglobin in increasing of the peroxidase activity of methaemoglobin.


1989 ◽  
Vol 98 (2) ◽  
pp. 455-462 ◽  
Author(s):  
Francisco J. Abajo ◽  
Maria Antonia S. Castro ◽  
Pedro Sánchez-García

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3747
Author(s):  
Weisheng Zhu ◽  
Luyao Wang ◽  
Qisi Li ◽  
Lizhi Jiao ◽  
Xiaokan Yu ◽  
...  

As one of the nanostructures with enzyme-like activity, nanozymes have recently attracted extensive attention for their biomedical applications, especially for bacterial disinfection treatment. Nanozymes with high peroxidase activity are considered to be excellent candidates for building bacterial disinfection systems (nanozyme-H2O2), in which the nanozyme will promote the generation of ROS to kill bacteria based on the decomposition of H2O2. According to this criterion, a cerium oxide nanoparticle (Nanoceria, CeO2, a classical nanozyme with high peroxidase activity)-based nanozyme-H2O2 system would be very efficient for bacterial disinfection. However, CeO2 is a nanozyme with multiple enzyme-like activities. In addition to high peroxidase activity, CeO2 nanozymes also possess high superoxide dismutase activity and antioxidant activity, which can act as a ROS scavenger. Considering the fact that CeO2 nanozymes have both the activity to promote ROS production and the opposite activity for ROS scavenging, it is worth exploring which activity will play the dominating role in the CeO2-H2O2 system, as well as whether it will protect bacteria or produce an antibacterial effect. In this work, we focused on this discussion to unveil the role of CeO2 in the CeO2-H2O2 system, so that it can provide valuable knowledge for the design of a nanozyme-H2O2-based antibacterial system.


1984 ◽  
Vol 429 (1 Biology and C) ◽  
pp. 604-606 ◽  
Author(s):  
SIEN YAO CHOW ◽  
JOHN W. KEMP ◽  
DIXON M. WOODBURY

1927 ◽  
Vol 46 (6) ◽  
pp. 935-956 ◽  
Author(s):  
Ann G. Kuttner

1. It has been shown that the guinea pig virus localizes in the submaxillary glands of young guinea pigs following subcutaneous, intraperitoneal, or intravenous injection of active material, and that the specific lesion is demonstrable in the glands in 12 to 15 days. When an active infection of the gland has been produced in this way, the guinea pigs are refractory to intracerebral inoculation of the virus. 2. No lesion develops in the submaxillary glands of young guinea pigs injected subcutaneously with guinea pig virus which has been inactivated by heat. Young guinea pigs which have received injections of heat-killed virus do not become refractory to intracerebral inoculation of the virus. 3. When young guinea pigs from which both submaxillary glands have been removed are injected subcutaneously with active virus, the virus localizes in the parotid gland, and the animals become refractory to intracerebral inoculation. 4. It has been impossible to demonstrate virucidal properties in the sera of adult guinea pigs which have become spontaneously infected with the virus, or in the sera of young guinea pigs which have been artificially rendered refractory to intracerebral inoculation. 5. It has been possible to transmit the virus from guinea pig to guinea pig continuously in series through seven animals by direct inoculation from submaxillary gland to submaxillary gland. 6. The fact that the virus regularly localizes in the submaxillary glands following subcutaneous inoculation has been utilized in passing the virus from guinea pig to guinea pig. 2 weeks after the subcutaneous inoculation of the virus into young guinea pigs, the active agent was present in the submaxillary glands. Emulsions of the submaxillary glands of these animals were then used for the subcutaneous injection of another group of young guinea pigs. In this way the virus was transmitted continuously from skin to submaxillary gland through a series of seven animals.


1956 ◽  
Vol 184 (2) ◽  
pp. 351-355 ◽  
Author(s):  
Frederick W. Maire ◽  
Harry D. Patton

The pulmonary edema which follows preoptic lesions in rats is prevented by antecedent bilateral section of the splanchnic nerves. Intravenous epinephrine in doses exceeding 0.0125 mg/100 gm body weight causes fatal lung edema in rats comparable to that produced by preoptic lesions. Moreover, extracted pressor amines from rat adrenal glands cause lung edema, often fatal, when injected into the donor or into intact rats. However, adrenal demedullation does not prevent lung edema following preoptic lesions. Hence the protective effect of splanchnectomy against preoptic lesions is not wholly due to adrenal denervation. It is tentatively suggested that preoptic lung edema results from overloading of the pulmonary circuit owing to splanchnic mediated constriction of visceral venous reservoirs. Liver and spleen weights of animals dying from preoptic lung edema were significantly less than normal.


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