Suspected zinc-induced copper deficiency in growing kittens exposed to galvanised iron.

AIM: To investigate the possible causes of fading coat colour and an acquired hind-limb ataxia affecting sixteen 4 to 5-month old kittens in a closed feline colony during 1993 and 1994. METHODS: Records of kittens and litters born in the colony between 1991 and 1997 were analysed. The kittens had been kept from birth until approximately 5 months of age in plastic cages with galvanised iron bar doors. Histopathological sections from 4 of the worst affected ataxic kittens necropsied in 1993 were re-examined. In addition, 6 of the original 16 affected kittens that survived were re-examined as 4 to 5-year old adults, which were moderately ataxic; these cats were then humanely killed for necropsy. RESULTS: In the kittens, clinical signs included lordosis, dysmetria, ataxia of the hind-limbs and fading coat colour; histopathological lesions included Wallerian-type degeneration in the spinal cord, pons and medulla, and neuronal degeneration in the vestibular nuclei and ventral horns of the spinal cord. Analysis of colony data ruled out an inherited disease, and there was no evidence of dietary inadequacy or excess. Similar, though milder, clinical and histopathological changes were noted in the affected adults. CONCLUSIONS: Circumstantial evidence is consistent with a diagnosis of zinc-induced copper deficiency caused by the ingestion of zinc oxide from the galvanised iron bar doors. CLINICAL RELEVANCE: Because of the possibility of zinc-induced copper deficiency, galvanised iron should be avoided when designing and constructing cages for cats in veterinary clinics, pet shops and boarding facilities.

Relationship between plasma testosterone and urinary felinine in the growing kitten.

Felinine, a unique amino acid the functions of which are not well understood, is found in large quantities in male cat urine. Our study ran for 13 calendar months and involved taking monthly samples of blood and urine from 10 male and 10 female kittens starting at 6 months of age and measuring urinary felinine and plasma testosterone concentrations. Felinine was detectable at 6 months of age in all cats (range, mean +/- SEM, nmol/mL, 13.8-801.1, 432.3+/-112.2, males and 34.3-393.0, 140.4+/-45.0 females). In entire males, felinine showed a biphasic pattern, peaking (2550 nmol/mL) between 11-13 months of age toward the end of the attainment of puberty then falling to a low (1048 nmol/mL) at 15 months of age then climbing to a peak (3661 nmol/mL) at 17 months of age. Natural plasma testosterone levels in entire males showed a similar biphasic pattern peaking (6.8 pmol/mL) at 12 months of age, falling (1.3 pmol/mL) at 15 months, and finally rising again (12.6 pmol/ml) at 16 months of age. Castration of half the male cats induced a parallel fall in both testosterone and felinine that was reversed following testosterone supplementation. Urinary felinine levels in entire females rose slowly throughout the study and reached 795 nmol/mL at 18 months of age compared to the level of 365 nmol/mL reached by the spayed females: these levels were not significantly different when expressed as felinine/creatinine ratios. We could not detect testosterone in either entire or spayed females and so concluded that felinine was unrelated to testosterone in these groups. There was strong evidence that plasma testosterone levels are positively correlated with urinary felinine levels in male cats. The control of felinine might be sex-linked and may be part of a pheromonal signaling process of the male cat.

Felinine: a urinary amino acid of Felidae.

Felinine (2-amino-7-hydroxy-5,5-dimethyl-4-thiaheptanoic acid) has been identified in the urine of several members of the Felidae family including the cat (Felis catus). Rates of excretion of 95 mg/day have been recorded for entire male cats with entire female cats excreting around 19 mg/day. These high excretion rates in entire male cats may have a significant effect on the daily sulphur amino acid requirement. The isoamyl moiety of felinine seems to originate from the same isoprenoid pool as used for the synthesis of cholesterol in the cat. The sulphur in the felinine molecule appears to originate from cysteine, although some contradictory evidence exists. The site of synthesis and the method of transportation in the blood remain largely unknown. The biological significance of felinine to the animal is still a matter for speculation, but its function as a precursor to a pheromone seems likely. Recently, an accurate chemical assay for felinine has been developed that will allow investigation of felinine in different tissues and excretions and from a wider range of mammals.

Twenty-four hour felinine [corrected] excretion patterns in entire and castrated cats.

The purpose of this study was to determine the 24 h urinary excretion of a sulphur containing amino acid called felinine in entire and castrated cats of both sexes. Entire male cats excreted (mean +/- SEM) 122 +/- 23.6 mmol of felinine per kg bodyweight per day with castrated males, entire females and spayed females excreting 41 +/- 8.4, 36 +/- 7.3 and 20 +/- 3.8 mmol, respectively. There was an overall significant difference between groups in the amounts of felinine excreted in 24 h [F(3, 24) = 11.8, p < 0.0001] with there being significant differences between entire males and castrated males (p < 0.001) and castrated males and spayed females (p < 0.05). There was no difference in excretion between entire and spayed females. Urine volumes were not significantly different for the 24 h period. The differences in excretion levels were caused by different concentrations of felinine in the urine with entire male cats excreting (mean +/- SEM) 2.0 +/- 0.55 g of felinine per litre of urine. The data obtained in the present study support the concept that felinine, which has been found in Felidae species only, may be testosterone dependent. Felinine may be involved in territorial marking.

Some effects of ovariectomy and estrogen replacement on body composition in the rat.

Sprague-Dawley rats were ovariectomized (OvX) at 3 ages, day 2 (D2), week 4 (W4) and week 7 (W7); a group of OvX W7 rats were treated daily with estrogen (OB;2 micrograms for 2 or 5 weeks from 10 weeks of age). Rats were slaughtered at 4 ages, weeks 7, 9, 12 and 15, for the chemical analysis of carcass and skin. Chemical compositions were analysed as % wet weight and as component weights by two-way analysis of variance. Component weights were also analysed by allometry, regressing against nose-anal length. Ovariectomy increased overall body weight without causing obesity. The weight gain of the OvX rat was mainly a true growth response but OvX affected body proportions so that at a given body length the OvX rat had a larger skin and carcass than controls. Ovariectomy at the earliest age (D2) produced the smallest response in body weight and body length but produced the greatest fat redistribution towards the skin and away from the carcass; there was no net change in whole body fat levels following OvX. Long-term daily OB treatment increased fat reserves but slowed the growth of other body components, including the axial skeleton. Whereas OvX redistributed components between skin and carcass, OB treatment reversed this process.

The linear regression of body weight and age in intact, ovariecotomised, and estrogen treated rats: some applications and implications.

Many variables, including rat body weight (BWt), are sequentially measured in individuals yet the information obtained is often poorly utilised. Many advantages result if a linear relationship is established, on the original or transformed scales, between the variable and time. For individual rats log BWt, which is normally distributed, is linearly related to the reciprocal of age. Slopes (rates of BWt gain) and constants (ultimate BWts) then serve as data. Linearity extended from 4 weeks onwards in ovariectomised (OvX) and intact rats, implying that puberty does not affect BWt and that BWt increases before puberty following pre-pubertal OvX; the ovary inhibiting growth before puberty. For individual rats weaning BWt was correlated with rate of BWt gain but not with ultimate BWt, indicating postweaning compensatory growth which continues to maturity. Pre-treatment and post-treatment measurements were made on individuals, allowing within-animal comparisons and regression. Thus the BWt response to OvX or estrogen treatment depended on the pre-treatment rate of BWt gain and ultimate BWt, implying that the BWt response entails a form of compensatory growth. OvX at three ages (day 2, week 4, and week 7) produced different rates of BWt gain but similar ultimate BWts. These results support the hypothesis that ultimate BWt is predetermined, but can be modified by treatment.

Effects of testosterone propionate treatment of neonatally ovariectomized rats on growth and subsequent responsiveness to oestrogen.

There was no significant difference in body weight between neonatally ovariectomized (OvX) rats whether given oil treatment or 90 mug testosterone propionate (TP) on day 3, when examined up to 23 weeks of age. When these two animals were injected with oestradiol benzoate (3 mug/day for 2 weeks), the neonatally OvX TP treated rats showed a significantly smaller depression in body weight than did the control neonatally OxX rats. Measurement of food intake also showed that TP treated rats responded significantly less to the depressant effects of oestrogen than did the controls. These data are consistent with the hypothesis that the ovary does restrain body weight in TP rats but that androgen treatment in the neonatal period may not have a specific effect on growth but may alter the sensitivity of growth regulating processes to the inhibitory effects of oestrogen.

Patterns of body weight change in rats following neonatal hormone manipulation: a "critical period" for androgen-induced growth increases.

The development of sexual behaviour and gonadal function is largely determined by the early postnatal hormone environment in the rat; testosterone propionate (TP) treatment in the neonatal female will stimulate development of predominantly masculine functional characteristics. On the other hand, removal of the testes from neonatal males results in feminization of these characteristics. It has been shown that an optimal neonatal steroid hormone environment is also essential for normal growth. We now report the effects of different doses of TP (10, 30, 90, or 270 mug) given on postnatal days 2, 3, 4, or 5 on growth as measured primarily by body weight. Only treatment in the 30-270 mug range on days 2 or 3 was effective in causing significant growth changes, however, these same doses caused sterility and impaired female sexual behaviour when given on days 4 or 5. Therefore, there appears to be a "critical period" before the fourth postnatal day when TP can affect processes leading to increased growth. Removal of the neonatal testes retards growth to the levels of the androgenized females. The ovaries of the female TP treated rats still have a restraining influence on growth since their removal produces an increment in body weight similar to, though not as great as, that of the normal ovariectomized rat. These findings suggest that neonatal TP administration may possibly reduce the responsiveness of rats to the growth depressing effect of ovarian steroids by action at a site functionally different from that producing sterility and impaired sexual behaviour.