Somdutta Sinha Roy

Identification of lutein, a dietary antioxidant carotenoid in guinea pig tissues.

Lutein, a dietary carotenoid, is a well known antioxidant. The major source of this carotenoid in humans is diet. We report here the presence of lutein, a dietary carotenoid in several guinea pig tissues (in decreasing order: liver>spleen>lung>>testis>kidney>plasma>eye but not in white adipose tissue). The presence of lutein in lung and other tissues may be significant in term of its antioxidant capacity of these organs.

Uptake of all-trans retinoic acid-containing aerosol by inhalation to lungs in a guinea pig model system—A pilot study

ABSTRACT Systemic therapies with retinoic acid (RA) can result in toxic side effects without yielding biologically effective levels in target tissues such as lung. The authors adapted a PARI LC Star nebulizer to create a tubular system for short-term inhalation treatment of guinea pigs using a water-miscible formulation of all-trans RA (ATRA) or vehicle. Based on the initial average weight, animals received an estimated average ATRA doses of either 0.32 mg·kg−1 (low dose, 1.4 mM), or 0.62 mg·kg−1 (medium dose, 2.8 mM), or 1.26 mg·kg−1 (high dose, 5.6 mM) 20 minutes per day for 6 consecutive days. This system led to a rise of ATRA levels in lung, but not liver or plasma. Cellular lung levels of retinol, retinyl palmitate, and retinyl stearate also appeared to be unaffected (245.6 ± 10.7, 47.4 ± 3.4, and 132.8 ± 7.7 ng·g−1 wet weight, respectively). The application of this aerosolized ATRA also induced a dose-dependent protein expression of the cellular retinol-binding protein 1 (CRBP-1) in lung, without apparent harmful side effects.

Breast cancer is associated with an increase in the activity and expression of cholinephosphotransferase in rats

AIM The present study aims to establish that cholinephosphotransferase (CPT), the terminal enzyme for the de novo biosynthesis of phosphatidylcholine (PC), can be used as a biomarker for breast cancer in an animal model. MAIN METHODS Breast cancer was induced by intragastric administration of dimethylbenz(a)anthracene (DMBA) in rats. The activity and expression of CPT were compared between normal breast tissues and breast tumors. To establish possible mechanistic model, we looked into other enzymes of PC biosynthesis as well as c-fos protein expression and DNA binding. KEY FINDINGS CPT enzyme activity and its expression were significantly higher in breast cancer tissues relative to normal breast tissues. Corresponding to the increase in the CPT activity and its expression, c-fos activity and its expression were also increased in breast tumors. SIGNIFICANCE The present study suggests that increased CPT activity and expression is associated with DMBA-induced breast cancer development.

Protection Against Dimethylbenz[a] Anthracene-Induced Breast Cancer in Female Rats by α-Lactalbumin.

Consumption of α-lactalbumin as dietary protein offers a beneficial effect on breast cancer development. Breast cancer was developed by gavage administration of single dose of dimethylbenz(a)anthracene (DMBA) in female rats, maintained on AIN-76A diet with either 20% casein or α-lactalbumin (a component of whey protein). All tumors were detected by palpation. After approximately 130 days of DMBA administration, the animals were euthanized. There was a delay in the development of breast tumor in the α-lactalbumin group in comparison to the casein group. The number of tumors per rat was less in the α-lactalbumin group than that in the casein group at any time point up to 130 days after DMBA administration. Also the incidence of tumors and tumor volume was less in the α-lactalbumin group than those in the casein group. The casein group had a mixture of grade I, grade II and grade III tumors whereas the α-lactalbumin group had mostly grade I tumor. Furthermore, the proliferative index was significantly lower in the α-lactalbumin group than that in the casein group.

Effects of intratracheal exposure of 2‐chloroethyl ethyl sulfide (CEES) on the activation of CCAAT‐enhancer‐binding protein (C/EBP) and its protection by antioxidant liposome

Exposure of 2‐chloroethyl ethyl sulfide (CEES) to guinea pigs causes lung injury by infiltration of neutrophils in interstitial lung spaces. A unique MAPK‐regulated transcription factor, C/EBP (CCAAT‐enhancer‐binding protein), regulates the expression of intracellular adhesion molecule‐1 (ICAM‐1), involved in recruiting neutrophils in lung. The present study was to determine if CEES exposure causes activation of C/EBP, in particular the predominant β‐isoform and if so whether it can be prevented by intratracheal delivery of an antioxidant liposome containing N‐acetyl cysteine and tocopherols. Lung injury was developed in guinea pigs by intratracheal exposure of CEES (0.5 mg/kg). The antioxidant liposome was given intratracheally 5 min after CEES exposure, and the animals were sacrificed after 30 days. CEES exposure caused a 2.3‐fold increase in the activation of C/EBP accompanied with a 45% and 121% increase in the protein level of C/EBP β and ICAM‐1, respectively, and this effect was counteracted by the antioxidant liposome.