Biomedical subjects

M J Yole

Publications and source records attributed to M J Yole.

4 recordsLinked to original sources

PubMed1999

Effect of chlorpyrifos on immune function in rats.

A commercial formulation of chlorpyrifos was evaluated for effects on selected immune system functions in male Fisher 344 rats. Chlorpyrifos in an olive oil vehicle was administered by oral gavage twice weekly for 28 d at a dose of 5.0 mg/kg for each treatment. Body weight and organ/body weight ratios were unaffected by the chlorpyrifos. In contrast, chlorpyrifos impaired T-lymphocyte blastogenesis induced by concanavalin A (P = 0.03) and phytohemagglutinin (P = 0.023), but did not alter B-lymphocyte blastogenesis induced by lipopolysaccharide/dextran (P = 0.082. Humoral immunity (anti-sheep red blood cell), a T-lymphocyte macrophage-dependent response, was also reduced (P = 0.019) when the antibody response was expressed/10(6) spleen cells, although the response expressed/spleen was unaffected (P = 0.32), reflecting increased lymphocyte production. The total splenic lymphocyte counts in the chlorpyrifos-treated rats increased by 91% (P < 0.0001), therefore reducing the antibody response when expressed/10(6) spleen cells. Chlorpyrifos had no effect on macrophage phagocytosis (P = 0.27), but increased the relative percentage expression of CD5+ (P = 0.028) and CD8+ (P = 0.003). The presence of normal antibody and phagocytic responses in association with reduced T-lymphocyte blastogenesis and enhanced expression of specific cell surface antigens indicated that chlorpyrifos induced immune alterations associated with lymphocyte subpopulations.

Animals↗

PubMed1998

Effect of pentachlorophenol on immune function.

The organochlorine compound, pentachlorophenol, was evaluated for effects on immune system function in male Fisher 344 rats. Pentachlorophenol was prepared in an olive oil vehicle and was administered by oral gavage twice weekly for 28 days at a dose of 2.0 mg/kg per treatment. Exposure to pentachlorophenol increased body weight gains (P=0.024) during the treatment period. Liver (P=0.034) and kidney (P=0.012) body weight ratios were also increased. Pentachlorophenol exposure enhanced T-lymphocyte blastogenesis induced by concanavalin A (Con A)(P=0.0001) and phytohemagglutinin (PHA)(P=0.048) evaluated using stimulation indices. Corresponding B-lymphocyte blastogenesis induced by lipopolysaccharide/dextran (LPS/dex)(P=0.0034) was also enhanced by pentachlorophenol exposure. Pentachlorophenol suppressed the antibody response against sheep red blood cells (SRBCs) by 39% when the response was expressed per viable spleen cell (P=0.006). This suppression was not evident when the response was expressed per spleen (P=0.22), suggesting that a compensatory mechanism or extramedullary splenic hemopoiesis was occurring minimizing the overall impact on humoral immunity. The enhanced B- and T-lymphocyte blastogenesis may also reflect compensatory or hemopoietic activity. Pentachlorophenol exposure had no effect on peritoneal macrophage phagocytosis (P=0.31) or lymphocyte cell surface antigen expression. The observed alterations in lymphocyte blastogenesis and humoral immunity subsequent to pentachlorophenol exposure do not appear to be associated with phagocytosis or lymphocyte cell surface antigen expression.

Animals↗

PubMed1998

Effect of 2,4-dicholorophenoxyacetic acid, trifluralin and triallate herbicides on immune function.

The commercial formulations of 3 commonly used herbicides (the amine salt of 2,4-dichlorophenoxyacetic acid, trifluralin and triallate) were evaluated for effects on immune function in male Fisher 344 rats. The herbicides were prepared in an olive oil vehicle and administered by oral gavage twice weekly for 28 d at the following doses: 10.0 mg 2,4-D/kg; 17.5 mg trifluralin/kg; 5.0 mg triallate/kg/treatment. Normal body weight and organ/body weight ratios indicated the rats tolerated the herbicide treatments without difficulty. Exposure to 2,4-D did not alter lymphocyte blastogenesis, 1 gm antibody production (anti-sheep red blood cell), lymphocyte cell surface marker expression or phagocytic function of peritoneal macrophages. Trifluralin acted as a weak mitogen, but impaired T-lymphocyte blastogenesis induced by phytohemagglutinin and concanavalin A. Other immunological measurements were unaffected by trifluralin exposure. Triallate exposure reduced peritoneal macrophage phagocytosis by 33%, showed weak mitogenic properties and impaired T-lymphocyte blastogenesis in the presence of phytohemagglutin. Triallate also increased the anti-sheep red blood cell response expressed/spleen by 43%, a phenomenon suggestive of a compensatory response to minimize the impact on overall immune function. The changes in lymphocyte or macrophage function due to the herbicide treatments were not associated with changes in lymphocyte cell surface antigen expression.

2,4-Dichlorophenoxyacetic Acid↗

PubMed1992

Systemic injections of alpha-1 adrenergic agonists produce antinociception in the formalin test.

The role of alpha 1 receptors in antinociception was investigated in the formalin test, a well established test of tonic pain. The effect of systemic injections of selective alpha 1-adrenergic agonists (phenylephrine and methoxamine), a mixed alpha agonist selective for alpha 2 receptors (ST-91), and 2 adrenergic antagonists (prazosin and idazoxan) was measured in groups of Long-Evans rats. All agonists tested produced significant antinociception in this test. Dose-response curves for each agonist were statistically parallel and equally efficacious (100% antinociception). Prior injection of 0.15 mg/kg prazosin (an alpha 1 antagonist) completely antagonized the antinociception produced by either an ED50 or a maximally effective dose of each agonist tested. Idazoxan (0.5 mg/kg), an alpha 2 antagonist, was without effect on the antinociception produced by phenylephrine or methoxamine. ST-91 produced significant antinociception in the presence of idazoxan although the response was different from that obtained with ST-91 alone. The observed antinociception in the formalin test was not due to drug-induced changes in peripheral inflammation as measured using plethysmometry. Moreover, none of the drugs tested produced significant changes in coordinated motor behavior (accelerated rotarod test) at doses that produced significant analgesia (ED50). We conclude that alpha 1 receptors contribute significantly to adrenergic analgesia in the formalin test by an undefined action on sensory processing mechanisms.

Adrenergic alpha-Agonists↗