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PubMed1987

Effect of seasonal changes in Leydig cell number on the volume of smooth endoplasmic reticulum in Leydig cells and intratesticular testosterone content in stallions.

Testes from 47 adult (4-20 years) stallions obtained in November-January (non-breeding season) and 41 adult stallions obtained in May-July (breeding season) were perfused with glutaraldehyde, placed in osmium and embedded in Epon 812. Percentage Leydig cell cytoplasm or nuclei in the testis was determined by point counting of 0.5 micron sections under bright-field microscopy. Testes from 6 randomly selected horses per season were processed for electron microscopy. The volume (ml) of SER/testis was calculated from the % SER in the cytoplasm % Leydig cell cytoplasm, and parenchymal volume. Number of Leydig cells was calculated from the % nuclei, parenchymal volume, histological correction factor, and volume of single nucleus. Intratesticular testosterone content was determined from the contralateral testis by radioimmunoassay. The volume of SER/g and testosterone/g tended to be higher in the breeding than non-breeding season. Leydig cell number/g, volume of SER/testis, testosterone/testis, and Leydig cell number/testis were significantly greater in the breeding than in the non-breeding season. Volume of SER/testis and testosterone/testis were related significantly to the cell number/testis, and SER/testis was related (P less than 0.05) to testosterone/testis. These results emphasize the importance of seasonal changes in the number of Leydig cells on the amount of SER available to produce testosterone and on testosterone content/testis in the stallion.

Animals↗
PubMed1982

Local differences in Leydig cell morphology in the adult rat testis: evidence for a local control of Leydig cells by adjacent seminiferous tubules.

In order to test the hypothesis that Leydig cell function in the adult rat testis is influenced by the surrounding tubules, Leydig cell morphology was compared in different types of interstitial areas. Triangular interstitial areas surrounded by 3 cross-sectioned tubules in nearly the same stage of spermatogenesis were chosen for quantitative light microscopy. It was found that the volume density of Leydig cells in such areas was about 30%, except when the surrounding tubules were in stages IX-X or XI-XII, when it was only about 20%. This variation in total Leydig cell mass seemed to be due to a variation in Leydig cell size and not in Leydig cell number. The largest Leydig cell profile area, 118 +/- 6 micrometers 2 (mean +/- SE n = 6 rats), was observed when the surrounding tubules were in stages VII-VIII, i.e. just prior to sperm release. The smallest Leydig cells were seen when the surrounding tubules were in stages IX-X and XI-XII (68 +/- 3 and 66 +/- 4 micrometers 2). The present results indicate that there may be a Leydig cell cycle in the adult rat testis, which is regulated by the adjacent tubules.

Animals↗
PubMed1976

Freeze-fracture observations on the intercellular junctions of Sertoli cells and of Leydig cells in the human testis.

Normal and feminized human testes were examined by means of freeze-fracture. In both cases, the junctional complexes between adjacent Sertoli cells show a unique characteristic feature. Many parallel linear occluding junctions are located circumferentially around the cell surface at the level of the nucleus. They are more than forty in number over one Sertoli cell surface. In the A face, the particles are not prominent on the ridge of the junctions. Instead, they are clearly seen in the center of the groove of the junctions on the B face. Gap junctions consisting of particle aggregation are not found between the Sertoli cells. The gap junctions between the Leydig cells are frequently observed in both normal and feminized testes. They are round or elliptic in contour and about several micrometers in diameter. The particles, about 8 nm in diameter, are closely packed to form a quasi-hexagonal pattern. The pits are found on the B face corresponding to the particle aggregation.

Adult↗
PubMed2000

Focal lobular spermatogenesis and pubertal acceleration associated with ipsilateral Leydig cell hyperplasia.

Leydig cell tumors of the testis are the underlying cause in about 10% of the cases of precocious puberty in boys. Leydig cell hyperplasia is a less well-characterized cause, with an undocumented frequency. We describe a boy with precocious puberty associated with ipsilateral testicular enlargement and focal Leydig cell hyperplasia with spermatogenesis limited to the local adjacent testicular tissue.

Biomarkers↗
PubMedDate not supplied

The actions of calcitonin on the TM3 Leydig cell line and on rat Leydig cell-enriched cultures.

Studies demonstrating calcitonin receptors on Leydig cells have suggested that these cells may be one of the many sites affected by this peptide. To investigate this possibility, the effect of synthetic salmon calcitonin on the TM3 Leydig cell line (derived from immature mouse Leydig cells) and on primary Leydig cell-enriched preparations was examined. Synthetic salmon calcitonin stimulated the conversion of [3H]adenine to [3H]cyclic AMP in TM3 cells. In addition, the hormone stimulated the basal secretion of testosterone in both TM3 cell- and Leydig cell-enriched cultures and potentiated the action of hCG on Leydig cell-enriched cultures. Synthetic salmon calcitonin also increased the concentration of androgen and estrogen receptors in cultured TM3 Leydig cells by 2- and 4-fold, respectively, when added to the culture medium (1 micrograms/ml). The fact that 8-bromo-cyclic AMP decreased both androgen and estrogen receptor concentrations suggested that the effect of calcitonin on sex steroid receptors is not mediated by its effect on cyclic AMP in these cells. The possibility that the action of calcitonin on steroid receptors might be mediated by another messenger such as calcium (Ca2+) was therefore considered. Progressively lowering the concentration of Ca2+ in the culture medium of the cells from 1.5 mM to less than 0.01 mM decreased the concentration of both androgen and estrogen receptors. Returning the Ca2+ concentration to normal levels (1.5 mM) restored steroid receptor levels. Receptor levels were also decreased when the extracellular Ca2+ concentration was lowered to 0.5 mM, and treatment with the Ca2+ ionophore, A23187 (1 microM), restored receptor levels to normal. The calcium channel blocker, verapamil, decreased the androgen receptor concentration but unexpectedly increased the concentration of estrogen receptors. It was concluded that calcitonin stimulates cAMP formation and testosterone secretion, and increases the concentration of sex steroid receptors. These observations provide evidence that the previously demonstrated calcitonin receptors on Leydig cells may be coupled to several biologic responses in this cell type.

Animals↗
PubMed1991

Interaction between cyclic nucleotide second messenger systems in murine Leydig cells.

Mouse Leydig cell androgen production can be acutely stimulated by atrial natriuretic factor (ANF) via cyclic guanosine 3',5'-monophosphate (cGMP). This stimulation can approach that seen with high concentrations of luteinizing hormone (LH) acting via cyclic adenosine 3',5'-monophosphate (cAMP). To assess the potential for synergistic interaction between LH/cAMP and ANF/cGMP Leydig cells were co-exposed to ANF and LH or ANF/cGMP and site/type-selective cAMP analogues. Co-exposure to 1 nM ANF and 1 ng/ml LH elicited a synergistic increase in androgen production. Both 500 microM 8-bromo-cGMP and ANF (1.0-2.5 nM) synergized with cAMP analogues selective for either of the two major isoenzymes of protein kinase A. Phosphodiesterase (PDE) inhibition was not involved as inclusion of a PDE inhibitor only augmented the response. It appears that ANF/cGMP may interact cooperatively with LH/cAMP in the stimulatory control of androgen production in the mouse Leydig cell and that the site of synergistic interaction may be the activation of the cAMP-dependent protein kinase.

Animals↗
PubMed1995

Hamster Leydig cells are less sensitive to ethane dimethanesulfonate when compared to rat Leydig cells both in vivo and in vitro.

It has been reported that ethane dimethanesulfonate (EDS) is a Leydig cell toxicant that affects rats and hamsters (Kerr et al., 1987), while, in contrast, the Leydig cells of mice are relatively insensitive to the toxicant. In the rat, there is a rapid decline in levels of testosterone (T) within hours after EDS administration. However, T production, spermiogenesis, and fertility are restored within a few weeks as new Leydig cells are formed from undifferentiated cells in the interstitium of the testis. In an earlier study, we found, as expected, that ejaculated sperm counts (ESCs) reached a nadir 10 days after adult rats were dosed with EDS at 65 mg/kg ip along with serum and testicular T, testis and seminal vesicle weights, and in vitro T production, while, in contrast, EDS at 65 mg/kg had no effect on these endpoints in the Syrian hamster (Gray et al., 1992). In the current study, when EDS was administered to 6, 12, and 18 month old hamsters at 100 mg/kg, it produced subtle effects on serum T and sex accessory gland weights, while dramatic effects were seen in similarly exposed rats. In addition, when testes were examined by light microscopy all treated rats displayed severely reduced Leydig cell numbers, while, in contrast, only one-third of the EDS-treated hamsters were affected, having moderately reduced Leydig cell numbers. In support of the histological data, 3 beta-HSD enzyme activity was reduced by 99% of control in EDS-treated rats, but it was reduced by only 35% of control in EDS-treated hamsters. An in vitro analysis of the effects of EDS on LH-stimulated T production by quartered testes demonstrated that the hamster testis was less sensitive to the direct effects of EDS than the rat testis. The IC50 after 3 hr in culture was greater than 1800 micrograms EDS/ml for the hamster quarter testes, while the IC50 for the rat quarter testes was 320 micrograms EDS/ml. In summary, these results demonstrate in vivo and in vitro that Leydig cells of hamsters are less sensitive to EDS than those of the adult rat.

Aging↗
PubMed1981

Lutropin-dependent protein phosphorylation and steroidogenesis in rat tumour Leydig cells.

Tumour Leydig cells have been incubated in the presence or absence of lutropin (luteinizing hormone, ;LH'). Stimulation of cells with lutropin (1000ng/ml) in the presence of 1-methyl-3-isobutylxanthine (0.25mm) resulted in increased steroid production and increased protein phosphorylation. When pregnenolone metabolism was inhibited, basal pregnenolone production was 26.9+/-7.4ng/60min per 10(6) cells; stimulated production was 156.1+/-39.5ng/60min per 10(6) cells (means+/-s.d., n=4). Lutropin-dependent phosphorylated proteins of molecular mass 17000, 22000, 24000, 33000 and 57000Da were detected. A significant increase of [(32)P]P(i) incorporation into these phosphorylated proteins was observed concomitant with the increased pregnenolone production. The occurrence of the phosphoproteins in nuclei, mitochondria and postmitochondrial-supernatant was investigated. The 17000Da phosphoprotein was found in the nuclear fraction, whereas the 22000, 24000, 33000 and 57000Da phosphoproteins were localized in the postmitochondrial-supernatant fraction. Of the cholesterol-side-chain-cleavage activity, 80.3+/-6.1% (mean+/-s.d., n=5) was present in the mitochondrial fraction isolated from tumour Leydig cells, and this activity was 2.5-fold increased when cells had been preincubated with lutropin/1-methyl-3-isobutylxanthine (basal production: 194.6+/-28.6ng/30min per mg of protein; lutropinstimulated production: 498.8+/-91.5ng/30min per mg of protein; means+/-s.d., n=3). The similarities in the kinetics of the phosphorylation of proteins and the pregnenolone production after addition of lutropin/1-methyl-3-isobutylxanthine indicate that the phosphoproteins could be involved in the lutropin-dependent increase in steroidogenesis in tumour Leydig cells. It remains to be demonstrated, however, to what extent the phosphoproteins outside the mitochondria can influence the cholesterol-side-chain-cleavage activity inside the mitochondria.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Stimulatory effects of methyltestosterone on pituitary gonadotropic cells and testes leydig cells of the three-spined stickleback, Gasterosteus aculeatus L., in winter.

Male three-spined sticklebacks were kept for a month in short photoperiod at ca. 20 degrees in winter. During this period methyltestosterone (MT), dissolved in the water (35 micrograms/liter), stimulated the appearance of breeding colors and kidney hypertrophy, characters which were both absent in the controls. MT furthermore prevented the onset of spermatogenesis. The gonadotropic cells of the MT-treated fish contained significantly more dilated endoplasmic reticulum and less granules than those of the controls. The nuclei of the testes Leydig cells were enlarged after treatment with MT. These findings suggest the existence of a positive feedback of androgen on the gonadal-pituitary axis of the male stickleback in winter.

Animals↗
PubMed1992

A partial characterization of a Sertoli cell-secreted protein stimulating Leydig cell testosterone production.

To examine whether immature rat Sertoli cells in culture secrete a factor(s) which stimulates testosterone production by mature mouse Leydig cells, Sertoli cell-enriched cultures were prepared from 3-week-old male rats with trypsin and collagenase. Sertoli cells were plated at an initial density of 3-5 x 10(6) cells/35 mm well and cultured in 3 ml serum free media supplemented with insulin (10 micrograms/ml). Sertoli cell culture medium (SCCM) collected every 3rd day was added to Leydig cells (10(6) cells in 1 ml of MEM with 2% steroid-free FCS) prepared from 10-week-old mice by mechanical separation and incubated for 3 h at 34 degrees C. Secreted testosterone was determined by RIA. SCCM 15 times concentrated by Amicon YM10 membrane demonstrated a dose-dependent stimulation of testosterone production, whereas there was no effect on testosterone secretion when Leydig cells were maximally stimulated by LH. Leydig cell stimulating activity was retained by both a dialysis membrane with a pore size of 24 A and an ultrafiltration membrane with a molecular weight cut-off of 10 kDa. However, activity was reduced by heating at 60 degrees C for 30 min and almost lost after incubation with 0.1% trypsin for 1 h at 37 degrees C. This activity was not retained by means of a Con A-Agarose column and was demonstrated only in break-through fractions. HPLC gel filtration of a 15 times concentrated SCCM preparation on a TSK gel G3000SW revealed Leydig cell-stimulating activity at approximately 13 kDa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Human chorionic gonadotropin protects Leydig cell function against 2,3,7,8-tetrachlorodibenzo-p-dioxin in adult rats: role of Leydig cell cytoplasmic volume.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters testicular steroidogenesis and reduces Leydig cell volume and number; however, human chorionic gonadotropin (hCG) stimulates testosterone production, increases the number and volume of Leydig cells and prevents TCDD's inhibition of testosterone production. The objective of this study was to determine if hCG protects Leydig cell function by maintaining sufficient Leydig cell cytoplasmic volume in TCDD-treated rats. Adult, male Sprague Dawley rats were divided into six treatment groups. Half of the animals received TCDD in corn oil (50 micrograms/kg body wt) and half received corn oil alone on Day 7 only. Additionally the rats received daily treatment of saline for 14 days, saline for 7 days and then hCG for 7 days, or hCG for 14 days. Rats were sacrificed on Day 14 and tissues collected. The decapsulated left testes were incubated in Eagles MEM for 2 h to determine basal production of testosterone and for 2 additional hours after the addition of hCG (100 IU) to the culture media. The right testis was evaluated by stereology to determine the volume of Leydig cells. Body weight was reduced (P < 0.01) in each TCDD-treated group; whereas, testicular weight was not affected by TCDD or hCG treatment. hCG prevented the TCDD-induced reduction in prostate and seminal vesicles weights. TCDD reduced the total volume of Leydig cell cytoplasm in saline-treated rats, but hCG eliminated the TCDD-induced reduction in Leydig cell cytoplasmic volume. hCG prevented the TCDD-induced reduction in Leydig cell function for both the 7- and 14-day treatments. Variation in the total volume of Leydig cell cytoplasm induced by the various treatment combinations was positively correlated with stimulated testosterone production in vitro (r = 0.486; P < 0.01) and the weight of the androgen sensitive organs (seminal vesicles, r = 0.562, P < 0.01; prostate, r = 0.380, P < 0.05). These data support the hypothesis that hCG prevents the TCDD-reduced Leydig cell function by maintaining sufficient Leydig cell cytoplasm and organelle content.

Animals↗
PubMed1998

Induction of Leydig cell tumors by lacidipine via up-regulation of the LHRH receptor on Leydig cells in rats.

Long-term (78 weeks) administration of lacidipine, a dihydropyridine calcium antagonist, increased the incidence of Leydig cell tumors (LCTs) in Sprague-Dawley rats. Lacidipine also increased and decreased the plasma luteinizing hormone (LH) and testosterone levels, respectively. Leydig cells from lacidipine-treated rats showed increases in luteinizing hormone-releasing hormone (LHRH) receptor expression, protein kinase C (PKC) activity, expression of proto-oncogenes, and 5-bromodeoxyridine uptake; whereas their calcium level, LH receptors, and testosterone content decreased. These data suggest that LHRH receptors play an important role in the development of rat LCTs induced by lacidipine, which activates a cascade of cell cycle-regulatory genes via PKC. When isolated Leydig cells were cultured with lacidipine or nicardipine, these changes in rat Leydig cells were not demonstrable in mice and monkeys, species having many fewer testicular LHRH receptors than rats. Thus, lacidipine may pharmacologically induce LCTs in rats but not in mice, with the difference depending on the presence or absence of testicular LHRH receptors. The induction of LCTs by lacidipine in rats is unlikely to occur in humans, since their Leydig cells lack LHRH receptors.

Administration, Oral↗
PubMed2001

Prolactin and Leydig cells: biphasic effects of prolactin on LH-, T3- and GH-induced testosterone/oestradiol secretion by Leydig cells in pubertal rats.

The effect of rat prolactin (rPRL) on basal and LH-, GH- and T3-mediated testosterone and oestradiol secretion was studied in pubertal rat Leydig cells. Purified Leydig cells were cultured for 24 h at 37 degrees C in a medium containing 4% foetal calf serum (FCS). The medium was then replaced with fresh medium containing different concentrations of rPRL (5-400 ng/mL) for 48 h at 34 degrees C without FCS. rPRL increased testosterone secretion by Leydig cells at doses of 50-400 ng and maximum stimulation was observed at a dose of 200 ng. Oestradiol secretion was parallel to that of testosterone except at low doses (5-50 ng/mL). To assess the modulatory effect of rPRL on LH-, GH- and T3-induced Leydig cell testosterone and oestradiol secretion, minimum (50 ng) and maximum (200 ng) effective doses of rPRL were co-administered with LH (25/100 ng), GH (10/50 ng) and T3 (25/50 ng). Co-administration of rPRL (50/100 ng) with T3 (25/50 ng) decreased testosterone secretion. While co-administration of T3 (25 ng) decreased rPRL-induced oestradiol secretion, the latter was unaltered at a dose of 50 ng T3. A minimum effective dose of rPRL (50 ng) plus LH (25 ng) stimulated both testosterone and oestradiol secretion. While a maximum effective dose of rPRL (200 ng) did not alter LH (25 ng)-induced testosterone and oestradiol secretion, it inhibited testosterone secretion induced by 100 ng LH and increased oestradiol secretion. Both doses of rPRL (50, 200 ng) plus GH (10/50 ng) inhibited testosterone secretion when compared with testosterone secretion induced by either GH or PRL alone and stimulated oestradiol secretion. The present in vitro study indicates that rPRL stimulates both testosterone and oestradiol secretion by Leydig cells and that this effect can be modulated by LH, GH and T3.

Animals↗
PubMed1995

A nonsense mutation of the human luteinizing hormone receptor gene in Leydig cell hypoplasia.

Leydig cell hypoplasia (LCH) is a form of male pseudohermaphroditism in which Leydig cell differentiation and testosterone production are impaired. This report describes the first case of a nonsense mutation (A1635C) in exon 11 of the human luteinizing hormone receptor (hLHR) gene in two sisters with LCH. This mutation causes loss of function of the receptor by introducing a stop codon at residue 545 in transmembrane helix 5 of the hLHR. Surface expression of the truncated hLHR (hLHR-t545) in human embryonic kidney cells stably transfected with cDNA encoding hLHR-t545 was diminished compared to the wild-type hLHR and hCG-induced cAMP accumulation was impaired. These results establish that single base mutations in exon 11 of the hLHR gene can produce inactivation as well as activation of the hLHR. Furthermore, they demonstrate that functional domains between transmembrane helix 5 and the C-terminal cytoplasmic tail of the hLHR are required for normal cell surface expression of the receptor and signal transduction.

Base Sequence↗
PubMed1994

Prolactin and testicular Leydig cell function: characterization of prolactin receptors in the murine MA-10 testicular Leydig cell line.

The direct role of prolactin (PRL) in testicular function is still unclear, mostly because of lack of a suitable in vitro model. To establish the suitability of the MA-10 murine tumor Leydig cell line for the study of PRL receptors (PRLR) and effects on steroidogenesis, we initially characterized PRLR on cultured MA-10 cells. The specific binding (Bs) of [125I]human growth hormone (hGH) depends on time, temperature, and Mg2+ ion and protein concentrations, with absolute specificity for the lactogenic hormones hGH and ovine PRL. Bs is saturable and is to a single class of high-affinity (Ka = 3.6 x 10(9) M-1) low-capacity (Bmax = 19.5 fmol/mg protein) binding sites. The molecular weight of PRLR, determined by cross-linking to [125I]hGH, SDS-PAGE and autoradiography, is 35 kDa for the free receptor, suggesting that the short-form PRLR protein, previously described in liver and mammary glands, is that primarily found in MA-10 cells. Thus, the demonstration of specific PRL binding sites on MA-10 Leydig cells, with characteristics similar to primary Leydig cell PRLR, suggests that this cell line can serve as a good model for both the study of PRLR mechanism of action and the role of PRL in Leydig cell function.

Animals↗
PubMed1995

Testicular serotonin is related to mast cells but not to Leydig cells in the rat.

Testicular serotonin (5HT) concentrations were determined by HPLC in the testes of rats treated neonatally with oestradiol benzoate (EB) and in adult rats treated with the Leydig cell cytotoxic ethylene dimethane sulphonate (EDS). 5HT concentrations were related to mast cell numbers. EB-treated rats showed an accumulation of mast cells in the testes at 35 and 70 days of age and increased 5HT concentrations in both the interstitial fluid and the testicular capsule, whereas no increases in 5HT concentrations or in the number of mast cells were found for the ventral prostate of these animals. On the contrary, 5HT concentrations were not related to the number of Leydig cells. In EB-treated rats, in which Leydig cells were nearly absent at 35 days of age, 5HT concentrations were significantly increased. Furthermore, EDS-treated rats did not show significant changes in 5HT concentrations, in spite of the elimination of Leydig cells. These data suggest that mast cells are a major source of serotonin in the rat testis.

Animals↗
PubMed2000

Short term regulation of cell-cell communication in TM3 Leydig cells. A perforated patch study.

Determination of the junctional conductance (g(j)) in TM3 Leydig cells by the dual whole cell patch clamp technique (DWCPC) shows that coupling undergoes a rapid and irreversible run down. Addition of ATP or cAMP derivatives to the pipette solution has been shown to prevent this phenomenon in several tissues, but this same treatment is unable to inhibit run down in Leydig cells. Because the run down in junctional conductance may pose serious problems to the interpretation of results, we also measured g(j) by using the double perforated patch clamp technique (DPPT). Access to the cell interior was achieved by adding 200 microgram/ml of nystatin to the pipette solution. With this method, run down in g(j) was greatly reduced, amounting to no more than 5% of the initial value. Exposure of the cells, under DWCPC or DPPT, to dibutyryl cAMP or to tumor promoting agent (TPA) led to a decrease in cell to cell communication. Staurosporine, a PKC inhibitor, increased g(j) and was able to prevent and reverse the uncoupling action of cAMP or TPA. Our results indicate that cell-cell communication in Leydig cells is down regulated by both protein kinases A and C, interacting in a complex manner.

Animals↗
PubMed2003

A constitutively active somatic mutation of the human lutropin receptor found in Leydig cell tumors activates the same families of G proteins as germ line mutations associated with Leydig cell hyperplasia.

Using a Leydig tumor cell line (MA-10) transiently transfected with the human lutropin receptor (hLHR) and mutants thereof, we examined the identity of the G proteins activated by the agonist-engaged hLHR-wild type (wt) and by three of its naturally occurring constitutively active mutants. Two of the mutants examined, L457R in transmembrane helix 3 and D578Y in transmembrane helix 6, are germ-line mutations found in boys with Leydig cell hyperplasia and precocious puberty. The third, D578H, is a somatic mutation found in Leydig cell tumors in boys with precocious puberty. We show that the hLHR-wt and the three mutants activate the G(s), G(i/o), and G(q/11), but not the G(12/13), families of G proteins. The activation of these G proteins by the hLHR-wt occurs only when engaged by agonist, but their activation by the L457R, D578Y, and D578H mutants occurs independently of agonist stimulation. We conclude that the G proteins activated by constitutively active mutants of the hLHR associated with Leydig cell hyperplasia or tumors are identical and are the same as those activated by the agonist-engaged hLHR-wt. If there was preferential activation of some G protein families by the somatic D578H mutation found in Leydig cell tumors as opposed to the germ line mutations found in Leydig cell hyperplasia, then one could envision mechanisms by which the D578H mutant would be oncogenic. The data presented here suggest that such mechanisms do not need to be considered.

Animals↗