tannic acid/necrosis

Tumor necrosis factor (TNF) induces hepatitis when injected in human beings or in rodents. The molecular mechanism by which TNF induces hepatic distress remains largely unknown, although induction of apoptosis of hepatocytes appears to be an essential step. In order to increase the therapeutic value

1. As early as 1hr. after the intraperitoneal administration of tannic acid to rats, it could be demonstrated in the liver. At 3hr. the nuclear fraction contained the largest amount of tannic acid. 2. Nuclear RNA synthesis was inhibited in vivo 2hr. after the administration of tannic acid. Induction

Tannic acid (TA) metabolism was studied in sheep after p.o., intra-abomasal and i.p. administration. TA and its phenolic metabolites in ruminal fluid, abomasal fluid, plasma and urine were determined using high-performance liquid chromatography at various intervals post-dosing. After po

As a consequence of human activity various toxicants reach the aquatic ecosystems; humics may interact with them and may change their toxicity. Many fish are exposed to a considerable concentration of humics and pollutants. Because of paucity of data on the biochemical action of tannins in the

A 13-week subchronic oral toxicity study of tannic acid (TA) was carried out in F344 rats at dose levels of 0, 0.025, 0.05, 0.1, 0.2 and 0.4% in the drinking water, to determine appropriate dose levels for a subsequent 2-year carcinogenicity study. The rats were randomly allocated to 6 groups, each

The effect of intraperitoneal administration of an aqueous solution of tannic acid was examined after different intervals of time. The results showed a gradual and progressive destruction of the liver cells and transformation of its architecture. The histological signs of liver damage appeared 2 hrs

Brucellosis is an emerging infectious disease affecting humans and animals. In this study, we investigated the in vitro and in vivo effects of tannic acid (TA) against Brucella abortus infection. After infection, F-actin polymerization and mitogen-activated protein kinases (MAPKs) (ERK 1/2 and p38α)

Acute tannic acid intoxication was studied in mice and sheep. In mice, following oral administration of 2.0 to 4.6 g of tannic acid kg-1 bodyweight, periacinar coagulative and haemorrhagic necrosis occurred in the liver. In sheep, following oral (8 g kg-1 bodyweight) administration of tannic acid,

The present study was performed to investigate the protective effects of tannic acid (TA) on liver injury induced by arsenic trioxide (ATO) and to elucidate the mechanism involved as related to the Kelch‑like ECH‑associated protein 1 (Keap1)‑nuclear factor erythroid 2‑related factor 2

Acute tannic acid toxicity was studied in 6 adult Merino ewes by administering 7-10% (w/v) tannic acid solution once into the abomasum via an abomasal fistula at dose rates of 0.5, 1.0 or 2.0 g tannic acid/kg body weight. Samples of blood, urine and abomasal fluid were collected over a 48-h period

Hydrolyzable tannins are known to exhibit diverse biological effects, which can be used in combination with silver nanoparticles (AgNPs). In this study, we tested toxic and inflammatory properties of tannic-acid modified 13, 33, 46 nm and unmodified 10-65 nm AgNPs using murine 291.03C keratinocyte

Tannic acid (TA) is a polyphenolic compound, which has shown diverse pharmacological effects with antimutagenic, anticarcinogenic and antibactericidal properties. However, cardioprotective effects of TA have not been reported. To investigate the protective effects of TA, rats were administered TA

Doxorubicin (DOX) is a highly effective drug, but its cardiotoxicity restricts its therapeutic index. Oxidative stress is the major etiopathological factor in DOX-induced cardiotoxicity. Tannic acid (TA) has various anti-cancer, antioxidant, and anti-inflammatory activities. The purpose of the study

Polyphenolic compound tannic acid, which is mainly found in grapes and green tea, is a potent antioxidant with anticarcinogenic activities. In this present study, we hypothesized that tannic acid could inhibit nuclear factor (NF)κB signaling and inflammation in atopic dermatitis (AD) NC/Nga mice. We