Verification of the Effectiveness of an SNP Marker in the Cholecystokinin Type A Receptor Gene for Improving Growth Traits in Okumino-kojidori Chickens.

A significant association was reported between a single nucleotide polymorphism (SNP; AB604331, g.420 C>A) in the cholecystokinin type A receptor gene and growth traits in some Japanese slow-growing chickens. Demonstration tests of the genetic improvement effect by comparing the superior allele-A fixed chickens with conventional ones were carried out considering the effect of different seasons on growth traits in other slow-growing chickens. Meat-type Okumino-kojidori chickens from Gifu Prefecture are a three-way cross of Gifu-jidori improved, White Plymouth Rock, and Rhode Island Red breeds. We used a total of 468 meat-type Okumino-kojidori: 264 individuals from a private hatchery as conventional chickens and 204 A-allele fixed individuals from the Gifu Prefectural Livestock Research Institute as improved chickens. We performed fattening experiments over two seasons: summer and winter. In each season, experimental birds of both sexes were hatched on the same day, raised in the same chicken house, and fed the same diet ad libitum for 12 weeks. Body weight was recorded at 3, 6, 9, and 12 weeks of age. SNP genotypes were determined using the mismatch amplification mutation assay. Association between the SNP and growth traits was analyzed using generalized linear models built on sex-based, seasonal, additive, and dominance genetic effects. The observed AA, AC, and CC genotype frequencies in the conventional chickens were 0.158, 0.479, and 0.363, respectively; body weight at 12 weeks and average daily gain from 3 to 12 weeks was superior for the A allele compared to the C allele. The improved chickens were heavier than the conventional ones at 12 weeks. Body weight at 12 weeks in allele-A fixed chickens increased by 3.2% compared to the conventional chickens. We concluded that g.420 C>A is a good selective marker that increases slaughter weight in the meat-type Okumino-kojidori chickens.

Microscopic analysis of the chromium content in the chromium-induced malignant and premalignant bronchial lesions of the rat.

OBJECTIVE: Our previous studies demonstrated that the frequency of gene instability in lung cancer of chromate workers was very high, but the frequencies of the p53 and ras gene mutations were low. To clarify the carcinogenesis of chromate in the lung, we established a chromate-induced cancer model in the rat proximal airway and examined the relationship between chromium accumulations and the chromium-induced cancer and premalignant bronchial lesions of the rat. METHODS: Fifteen male, bred, 12-week-old Jcl-Wister rats were used. A pellet of strontium chromate were inserted into the bronchus of the rats. The rats were sacrificed 9 months after the pellet was inserted. We pathologically examined the region of the bronchi to which the pellet was attached. We quantified the amount of chromium accumulation in the bronchial lesions using a microscopic X-ray fluorescence analyzer. RESULTS: Of the 15 rats, 1 rat had a lesion of squamous cell carcinoma (SCC), 7 rats had carcinoma in situ (CIS) or dysplasia, 8 rats had squamous metaplasia, and 5 rats had goblet cell hyperplasia. The amounts of chromium accumulation in normal epithelium (n=24), goblet cell hyperplasia (n=14), squamous metaplasia (n=8), and dysplasia plus CIS plus SCC (n=9) were 500+/-1354, 713+/-1062, 941+/-1328, and 3511+/-4473 (mean+/-SD) counts/s/mA, respectively. The amount of chromium accumulation was significantly increased according to the progression of malignant change of the bronchial epithelium (Spearman's correlation coefficient by ranks, rs=0.454, P<0.01). CONCLUSIONS: The amount of chromium accumulation was significantly increased according to the progression of malignant change of the bronchial epithelium. Examining the genetic alterations of histologic changes in this model was helpful in elucidating the process of carcinogenesis of chromium in the lung.

Microscopic analysis of chromium accumulation in the bronchi and lung of chromate workers.

BACKGROUND: It is known that chromium is an inhaled carcinogen and an important risk factor in the development of lung carcinoma. METHODS: The authors used a microscopic X-ray fluorescence analyzer with transmitted X-ray mapping imaging (Horiba, Kyoto, Japan) to measure the accumulation of chromium in 10 resected lung tissue specimens and 90 biopsy specimens from chromate workers. RESULTS: The maximum chromium accumulation (mean +/- standard deviation) in 10 resected lung tissue specimens was 197 +/- 238 counts per second (cps)/mili ampere (mA) (range, 4-649 cps/mA). Chromium accumulation was scattered in six tissue specimens and diffuse in one specimen. Chromium accumulation in the proximal bronchi was less than in the bronchioles or subpleural regions of the lung. Chromium accumulation was detectable in 63 (70%) of 90 biopsy specimens, and the mean accumulation was 6.5 +/- 9.2 cps/mA (range, 0-46.5 cps/mA). Chromium detected in bronchial tissue specimens was deposited in the bronchial stroma but not in the epithelium. The maximum chromium accumulations in dysplasic (n = 3), squamous metaplastic (n = 10), and normal bronchial epithelia (n = 9) in chromate workers and in normal bronchial epithelia (n = 3) in non-chromate workers were 20.2 +/- 5.4, 18.3 +/- 12.2, 13.2 +/- 13.4, and 3.0 +/- 1.8 cps/mA, respectively. The amount of chromium accumulation significantly increased according to the progression of malignant change of the bronchial epithelium (P = 0.003). CONCLUSIONS: Previous studies found that lung carcinoma with chromate exposure exhibited a variety of genetic abnormalities. Considering genetic aberrations and chromium accumulation in these premalignant lesions is useful for elucidating the process of carcinogenesis in chromium-induced lung carcinoma.