Colchicine antimitosis causes progression of S-(1,2-dichlorovinyl)-l-cysteine-induced injury leading to acute renal failure and death in mice

Reddy, Ramesh N.; Latendresse, John R.; Mehendale, Harihara M.

doi:10.1016/j.tox.2005.12.012

Cited by 9 publications

(4 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The parenteral colchicine dose used herein was consistent with colchicine dosing in other murine studies (46)(47)(48), but higher than that used to treat gout in humans. However, a single dose is likely to be better tolerated than repeated dosing over many days.…”

Section: Figuresupporting

confidence: 63%

Colchicine inhibits pressure-induced tumor cell implantation within surgical wounds and enhances tumor-free survival in mice

Craig¹,

Owen²,

Conway³

et al. 2008

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Figuresupporting

confidence: 63%

Colchicine inhibits pressure-induced tumor cell implantation within surgical wounds and enhances tumor-free survival in mice

Craig¹,

Owen²,

Conway³

et al. 2008

J. Clin. Invest.

View full text Add to dashboard Cite

“…The proliferating cell nuclear antigen (PCNA) is an auxiliary protein for DNA delta polymerase that is essential for DNA replication, DNA repair and chromatin remodeling in noncycling cells [28] . It has been reported that colchicine inhibited PCNA expression in mice renal tissue [29] . Bumbasirevie et al (1996) [30] reported that colchicine resulted in cell death of cultured lymphocytes.…”

Section: Discussionmentioning

confidence: 96%

Effect of Colchicine administration on the structure of the Spleen of adult male albino rat: Histological and Immunohistochemical study

Bekheet

2019

Egyptian Journal of Histology

View full text Add to dashboard Cite

Background:Colchicine is a natural alkaloid derived from autumn crocus; it is used in the treatment of gout and in preventing familial Mediterranean fever attacks. It accumulates in many organs such as spleen and may lead to their damage. Aim: This work aimed to study short and long duration effects of colchicine administration on the structure of the spleen of the adult male albino rat. Material and Methods: Forty-five adult male albino rats were used in this study, aged from 4-6 months, weighting 150 -180 gm. Rats were equally divided into three groups: Group I: It was further equally subdivided into three subgroups: subgroup IA: Kept as a negative control, subgroup IB: received 1ml of distilled water/day orally for seven days and subgroup IC: received 1ml of distilled water/day orally for 30 days. Group II: received 3mg/Kg body weight/ day of colchicine orally for seven days. Group III: received colchicine as those of group II but for 30 days. Results: The present work revealed that administration of colchicine for short duration induced mild structural alteration of rat's spleen in the form of reduction in lymphoid follicles size and subcapsular congestion of blood vessels, while, marked structural alteration of rat's spleen was noticed in group III that received colchicine for long duration in the form of loss of distinction between the white and red pulps with nearly unidentifiable lymphoid follicles and marked parenchymal congested blood vessels. Conclusion:Colchicine administration induced structural alteration of rat's spleen which was mild with short term use and extensive with long term use.

show abstract

“… 1 Extensive research over the last several decades has revealed that CTR plays a crucial role in determining the fate of the initiated injury. 1 , 36 - 44 Quick onset of adequate CTR, as in the case of low to moderate dose of toxicants, leads to the regression of injury. 45 , 46 On the other hand, lethal dose treatment causes suppression of the CTR giving a freeway for the unabated expansion of the initiated injury.…”

Section: Discussionmentioning

confidence: 99%

“…1 Extensive research over the last several decades has revealed that CTR plays a crucial role in determining the fate of the initiated injury. 1,[36][37][38][39][40][41][42][43][44] Quick onset of adequate CTR, as in the case of low to moderate dose of toxicants, Figure 5. (A) Representative Western blot images for hepatic total c-Jun N-terminal kinases (JNK), phospho-JNK, and Cyp2e1 expression at 1, 6, and 24 hours in the TA24 þ NaCl-, DW24 þ APAP-, and TA24 þ APAP-treated mice with (B) respective densitometric analysis.…”

Section: Discussionmentioning

confidence: 99%

Wnt/β-Catenin Signaling Drives Thioacetamide-Mediated Heteroprotection Against Acetaminophen-Induced Lethal Liver Injury

et al. 2017

Self Cite

View full text Add to dashboard Cite

Preplacement of compensatory tissue repair (CTR) by exposure to a nonlethal dose of a toxicant protects animals against a lethal dose of another toxicant. Although CTR is known to heteroprotect, the underlying molecular mechanisms are not completely known. Here, we investigated the mechanisms of heteroprotection using thioacetamide (TA): acetaminophen (APAP) heteroprotection model. Male Swiss Webster mice received a low dose of TA or distilled water (DW) vehicle 24 hours prior to a lethal dose of APAP. Liver injury, tissue repair, and promitogenic signaling were studied over a time course of 24 hours after APAP overdose to the TA- and DW-primed mice (TA + APAP and DW + APAP, respectively). Thioacetamide pretreatment afforded 100% protection against APAP overdose compared to 100% lethality in the DW + APAP-treated mice. Although hepatic Cyp2e1 was similar at the time of APAP administration, immediate activation of hepatic c-Jun N-terminal kinases (JNK) was observed in the TA + APAP-treated mice compared to its delayed activation in the DW + APAP group. In contrast to the DW + APAP group, the TA + APAP-treated mice exhibited extensive CTR, which was secondary to the timely activation of Wnt/β-catenin pathway. Our data indicate that rapid activation and appropriate termination of Wnt/β-catenin signaling and modulation of JNK activity underlie TA + APAP heteroprotection.

show abstract

Colchicine antimitosis causes progression of S-(1,2-dichlorovinyl)-l-cysteine-induced injury leading to acute renal failure and death in mice

Cited by 9 publications

References 40 publications

Colchicine inhibits pressure-induced tumor cell implantation within surgical wounds and enhances tumor-free survival in mice

Colchicine inhibits pressure-induced tumor cell implantation within surgical wounds and enhances tumor-free survival in mice

Effect of Colchicine administration on the structure of the Spleen of adult male albino rat: Histological and Immunohistochemical study

Wnt/β-Catenin Signaling Drives Thioacetamide-Mediated Heteroprotection Against Acetaminophen-Induced Lethal Liver Injury

Contact Info

Product

Resources

About