Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.5 (cathepsin D)
 4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hair follicles exhibit an intrinsic hair cycle that is divided into three phases; growth (anagen), transition (catagen) and quiescence (telogen). To make sure of the effects on hair growth by chemical substances, we should evaluate the induction of the anagen phase and/or elongation of the anagen period and delay in catagen separately, but the regulatory mechanism of the hair cycle is unclear. We have investigated the levels of biochemical markers in the third hair cycle period of C3H mouse (8 weeks, male) after depilation and compared them with those in a non-treated group. The dorsal areas (2 cm x 4 cm) were clipped and depilated with hair remover. The dorsal skin samples were collected 1, 8, 11, 15 and 18 days after depilation and the levels of biochemical markers, i.e. skin transglutaminase, skin sulfhydryl oxidase, cathepsin D, gamma-glutamyl transpeptidase, alkaline phosphatase, acid phosphatase, tyrosinase activities and histamine content in each skin sample were examined. The levels of gamma-glutamyl transpeptidase, tyrosinase and alkaline phosphatase were relevant to hair re-growth in the control group, but not skin transglutaminase, skin sulfhydryl oxidase, cathepsin D activities. The histamine content increased just after depilation treatment and returned to the normal level within two weeks, compared with the non-treated group. All these results suggest that the markers examined in this C3H mice model are useful for studying the distinctive process of hair re-growth caused by active substances.
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PMID:Evaluation of biochemical indices as a hair cycle marker in C3H mice. 884 Jan 42

The role of lipid peroxidation (LPO) in renal tubular damage mediated calcium oxalate retention was investigated in a rat model. Hyperoxaluria, without deposition of oxalate in kidney, was induced by administration of ethylene glycol (EG), a precursor of oxalate. Oxidative stress condition was produced by administration of buthionine sulfoximine (BSO), an inhibitor of glutathione biosynthesis. BSO-treated rats showed a significant (p < 0.001) increase in LPO over EG-treated rats and it was almost doubled in BSO + EG treated rats. LPO was accompanied by significant urinary excretion of renal damage marker enzymes such as gamma-glutamyl transpeptidase (gamma-GT), alkaline phosphatase (ALP) and cathepsin D, mucoproteins, and glycosaminoglycans (GAGs) in the BSO and BSO + EG groups but not in the EG group. Urinary excretion of gamma-GT (r = +0.90) (p < 0.001) and deposition of oxalate (r = +0.78) (p < 0.001) in kidney positively correlated with LPO. These results suggest that LPO initiates renal damage, thereby leading to calcium oxalate retention and stone formation.
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PMID:Renal injury mediated calcium oxalate nephrolithiasis: role of lipid peroxidation. 915 57