Population dynamics of the feral macaques in the Kowloon Hills of Hong Kong.

Hong Kong's feral monkey population is controversial. Many people complain about the aggressiveness of the monkeys, while some conservationists urge the government to deal with the problem in a way that will not harm the monkeys. The population dynamics of the macaques in the Kowloon Hills were studied in 1992 and 1993. Vital statistics are provided from this study as a first step in resolving the problems of human provisioning and wildlife management. It is unlikely that these macaques are indigenous to the area. They are the descendents of macaques that were released in the early twentieth century to control the spread of a local poisonous plant, the strychnos, which contains alkaloids poisonous to livestock and humans but which is a favorite food of the macaques. The macaque population expanded dramatically during the 1980s. The census method employed in this study is direct head count and photo-identification. At the end of 1993, the estimated abundance was 690 (+/-6) in eight social groups in the Kowloon Hills. Species found were rhesus (Macaca mulatta) 65.3%, longtailed (M. fascicularis) 2.2%, Tibetan (M. thibetana) 0.2%, and hybrids 32.3%. The overall home ranges occupied 2.15 km2, resulting in a very high macaque density of 326 per km2. The birth rates were 56.9% and 69.4% in 1992 and 1993, respectively. Mean adult sex ratio (M:F) was 1:2.2 for social groups and 1:1.6 including all peripheral males. The main mortality factor was road accidents and these contributed to the "missing rate" of 9.8% and 10.6% in 1992 and 1993, respectively. Population growth was 5.6% in 1992 and 7.8% in 1993. The estimated macaque population in the year 2000 will be around 1,100 if conditions remain favorable. Management strategies are recommended.

Distribution of plasma phosphatidylcholine molecular species in rabbits fed fish oil is modulated by dietary n-6 fatty acids.

The present study examined the distribution of plasma phosphatidylcholine (PC) molecular species in rabbits fed a chow diet supplemented with fish oil (FO) in combination with either hydrogenated coconut oil or the n-6 fatty acid-rich evening primrose oil (EPO) for 4 weeks. Significant proportions of plasma PC molecular species contained long-chain n-3 fatty acids. Addition of EPO to the FO supplemented diet increased the incorporation of n-6 fatty acids into plasma PC molecules; it also raised the proportions of 16:0-18:2, n-6, 18:1-18:2, n-6, 18:2, n-6-18:2, n-6, and 16:0-20:4, n-6. The increase of n-6 fatty acid-containing PC was at the expense of n-3 fatty acid containing PC species. However, feeding n-6 fatty acids did not affect the distribution of PC molecular species based on total carbon chain length. The most interesting observation was that dietary suplementation with EPO, raised the ratio of 22:6, n-3-containing to 20:5, n-3-containing molecular species, suggesting an enhanced conversion of 20:5, n-3 to 22:6, n-3.

Low susceptibility of nude mice to induction of invasive urinary bladder cancers by N-ethyl-N-(4-hydroxybutyl)nitrosamine.

A time- and dose-dependent study of N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN) bladder carcinogenesis was performed in nude mice maintained on tap water containing 0.025% EHBN for 4, 12, and 20 weeks ad libitum. A total of 13 invasive tumors, comprising 11 transitional cell carcinomas (TCCs) (84.6%) and 2 squamous cell carcinomas (SCCs) (15.4%), were found. Compared with previous results for B6C3F1 mice exposed to the same EHBN insult, the numbers of invasive carcinomas induced in nude mice, and especially of SCCs, were low. In order to ascertain whether this difference in cancer incidence between nude and B6C3F1 mice was due to variation in urinary excretion, the metabolism of EHBN was also investigated and compared with that of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN). Respective total urinary excretions over 48 hr of N-ethyl-N-(3-carboxypropyl)nitrosamine (ECPN) or N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), the ultimate carcinogenic species of EHBN or BBN, were 822.4 +/- 41.4 micrograms and 530.4 +/- 81.0 micrograms, respectively, in nude mice, and 800.6 +/- 83.7 micrograms and 407.8 +/- 69.7 micrograms, respectively, in B6C3F1 mice. In conclusion, although it is apparent that nude mice have a low susceptibility to EHBN induction of urinary bladder cancer, this does not appear to be dependent on reduced metabolism to the active form.

Polycyclic aromatic hydrocarbons in harp seals (Phoca groenlandica) from the Northwest Atlantic.

There is virtually no information available on concentrations of polycyclic aromatic hydrocarbons (PAH) in seals from any of the world's oceans. The largest harp seal population in the world is found in Canadian waters of the Northwest Atlantic. Samples of muscle tissue obtained from twenty eight harp seals ranging in age from foetuses to animals 22 years old were analyzed for total PAH and lipid content. Concentrations were determined in terms of crude oil and chrysene equivalents in line with recommendations of the International Oceanographic Commission. Overall, relatively low concentrations were found, the highest values being less than 1 ppm (microgram/g) in terms of chrysene equivalents and 4 ppm (microgram/g) in terms of petroleum hydrocarbon equivalents. The lowest concentrations were observed in fetal tissue. There was no evidence of bioaccumulation with age, the concentrations in juvenile seals (1-5 years) being higher than concentrations in older animals (6-20 years). There was also no correlation between PAH concentration and fat content. There is a possibility that the animals having elevated levels of PAH are from the Gulf of St. Lawrence herd, indicating the importance of obtaining more information on PAH levels in marine mammals and other organisms from this and similar regionally contaminated seas.

Bile acids from the harp seals, Phoca groenlandica.

1. The bile acids composition of the harp seal, Phoca groenlandica, collected around Newfoundland, Canada, had been examined. 2. 13C n.m.r. spectroscopy of the crude bile extract was superior to t.l.c. analysis in revealing the presence of phocaecholic acid and a taurine moiety in this mixture. 3. The relative percentage of cholic, phocaecholic and chenodeoxycholic acids was 60.5% (+/- 4.5), 21.4% (+/- 4.0) and 18.1% (+/- 5.8), respectively. 4. The variation in the percentage of bile acids did not correlate with the sex of the sampled animals, but varied significantly with the age of the seals.

Hepatocarcinogenic activities of hydroxymethyl derivatives of 4-(N,N-dimethylamino)azobenzene in ACI/N rats.

The hepatocarcinogenic potencies of three newly identified hydroxymethyl derivatives of 4-(N,N-dimethylamino)azobenzene [(DAB) CAS: 60-11-7], i.e., 2'-CH2OH-DAB, 3'-CH2OH-DAB, and 4'-CH2OH-DAB, were strictly evaluated in a long-term test (400 days) and compared to the potency of 3'-CH3-DAB. ACI/N rats, known to be less sensitive to azo dye carcinogenesis, were given one of these compounds in their diets for 120 days. The incidence of hepatocellular carcinoma in group 2 (20/20), which was given 3'-CH2OH-DAB, was much higher than that in any of the other groups: group 1 (2'-CH2OH-DAB; 4/19), group 3 (4'-CH2OH-DAB; 1/25), or group 4 (3'-CH3-DAB; 3/24). These data suggest that 3'-CH2OH-DAB is the most potent hepatocarcinogen in the series of azo dyes. Possible reasons for the potency of the chemical are discussed.

Genotoxicity of a variety of azobenzene and aminoazobenzene compounds in the hepatocyte/DNA repair test and the Salmonella/mutagenicity test.

Genotoxicity of 39 azo dye compounds of azobenzenes, aminoazobenzenes, and diaminoazobenzenes was examined in the hepatocyte primary culture/DNA repair test. Azobenzene (AzB) and 3,3'- or 4,4'-substituted azobenzenes such as (CH3)2AzB, (CH2OH)2AzB, (CH2OCOCH3)2AzB, and (CH2Cl)2AzB did not generate DNA repair, indicating lack of genotoxicity of these compounds. In contrast, all of 24 aminoazobenzenes, including those of unknown carcinogenicity, i.e., 3'-methyl-4-aminoazobenzene, 3'-CH2OH-aminoazobenzene, 3'-hydroxymethyl-N-methyl-4-aminoazobenzene, 3'-COOH-methylaminoazobenzene, 4'-formyl-N,N-dimethyl-4-aminoazobenzene, 3'-CH2Cl-dimethylaminoazobenzene, 4'-CH2Cl-dimethylaminoazobenzene, and 2'-, 3'-, or 4'-CH2OCOCH3-dimethylaminoazobenzene, elicited DNA repair synthesis. A positive DNA repair response was obtained for the 3 of 6 tested diaminoazobenzenes, i.e., N'-acetyl-N'-methyl-4-amino-dimethylaminoazobenzene, N'-acetyl-N'-methyl-4-amino-methylaminoazobenzene, and N'-acetyl-N'-methyl-4-amino-N-acetyl-methylaminoazobenzene, which are known to be carcinogenic. These results indicate that the amino group is functional for the expression of genotoxicity of azobenzene compounds. Twenty-one azobenzenes of these 3 classes were also examined for their mutagenicity in the Salmonella/mutagenicity assay. These results were almost identical with those of the DNA repair test except for several azo dyes such as AzB and 4,4'-(CH2Oacetyl)2AzB of the azobenzenes and N'-acetyl-4-amino-dimethylaminoazobenzene and N'-acetyl-N-methyl-4-amino-N-acetyl methylaminoazobenzene of the diaminoazobenzenes.